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        <title>Archivum Immunologiae et Therapiae Experimentalis Feed</title>
        <link>https://reference-global.com/journal/AITE</link>
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            <title>Archivum Immunologiae et Therapiae Experimentalis Feed</title>
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            <link>https://reference-global.com/journal/AITE</link>
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        <copyright>All rights reserved 2026, Hirszfeld Institute of Immunology and Experimental Therapy</copyright>
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            <title><![CDATA[Single-Nucleus Transcriptomics Reveal Mechanisms of Cardiovascular Protection Against Ponatinib-Induced Cardiotoxicity Through ROCKs Deletion in Cardiomyocytes]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0027</link>
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            <pubDate>Fri, 30 Oct 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Ponatinib is a potent tyrosine kinase inhibitor and primarily used in the treatment of chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph + ALL). Its broad anti-cancer capability is restricted to CML or Ph + ALL harboring T315I mutant breakpoint cluster region gene fused with the Abelson murine leukemia gene 1 due to its potential cardiotoxicity (CTX) side effect. It is crucial to better understand the mechanisms of ponatinib’s CTX to maximize its beneficial therapeutic effects while reducing CTX. We established a ponatinib-induced CTX mouse model, which was used in this study for evaluating long-term effects of ponatinib on cardiac structure and function. We first assessed the role of Rho-associated coiled-coil containing kinases 1 and 2 (ROCK1 and ROCK2) in mediating CTX on mouse models characterized by the inducible cardiomyocyte-specific double ROCK knockout (DKO). Next, we expanded the study with single nucleus RNA sequencing (snRNA-seq) to reveal critical differentially expressed genes and interrelated biological pathways. Finally, we hypothesized the most probable underlying cellular and molecular mechanisms by synthesizing the mouse model and transcriptomic findings. Important findings include that double ROCK deletion in cardiomyocytes prevented ponatinib-induced cardiac dilation and dysfunction and suppressed serum levels of several vascular toxicity biomarkers. Analysis of snRNA-seq revealed cell-type-specific transcriptomic signatures attributable to ponatinib treatment; however, they were attenuated in DKO mouse hearts. The associated genes include extracellular matrix- and thrombogenesis-related genes in cardiomyocytes, myofibroblast activation-related genes in fibroblasts, and pathological activation-related genes in endothelial cells (EC). The hypothesized mechanism is to integrate transcriptomic signatures of these three functional associated cell types with prior established roles of ROCK1 and ROCK2 in regulating actin cytoskeleton rearrangement. Hence, the contributory roles of cardiomyocyte ROCK in CTX and vascular toxicity have opened a new field for future experimental validation: drug-activated ROCK activities and cytoskeleton reorganization occurred in cardiomyocytes, fibroblasts and EC form the driving forces responsible for CTX induction.]]></description>
            <category>ARTICLE</category>
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        <item>
            <title><![CDATA[Ectromelia Virus Reprograms the Noncanonical NF-κB Signaling Pathway in HeLa Epithelial Cells]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0025</link>
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            <pubDate>Sun, 18 Oct 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[The noncanonical nuclear factor κB (NF-κB) pathway regulates adaptive immune responses and antiviral innate immunity. Orthopoxviruses, including the human pathogen variola virus and zoonotic viruses such as vaccinia virus and monkeypox virus, have evolved multiple strategies to suppress host antiviral signaling. Our previous work using in vitro immune cell models demonstrated that the mouse-specific orthopoxvirus ectromelia virus (ECTV) inhibits the noncanonical NF-κB signaling pathway. Here, we investigated the impact of ECTV on noncanonical NF-κB signaling in human epithelial HeLa cells. Tumor necrosis factor superfamily ligands were used to activate or modulate noncanonical NF-κB signaling. Using fluorescence microscopy and immunoblot analyses, we found that ECTV reduced LIGHT (TNFSF14)- and lymphotoxin α1β2 (LTα1β2)-induced nuclear accumulation of the NF-κB subunits RelB and p52. ECTV infection alone increased whole-cell RelB and NF-κB2/p100 levels but did not significantly alter nuclear RelB levels. In TNF-α-stimulated cells, ECTV reduced levels of cellular inhibitor of apoptosis protein 2 (cIAP2), whereas in LTα1β2-stimulated cells, ECTV reduced levels of TNF receptor-associated factor 3 (TRAF3). RT-qPCR analysis revealed that ECTV upregulated RELB, NFKB2, and CHUK expression. Viral infection also increased expression of TNFAIP3 and OTUD7B, genes encoding regulators of noncanonical NF-κB signaling. Moreover, infected cells exhibited increased expression of selected RelB-responsive genes, including FBRS, CCR10, and TNFRSF6B. Together, these findings indicate that ECTV modulates components associated with noncanonical NF-κB signaling in epithelial cells in vitro, without evidence of constitutive pathway activation.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Natural Killer Cells in Kidney Transplantation: Dual Role in Allograft Injury and Immune Adaptation]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0026</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0026</guid>
            <pubDate>Wed, 30 Sep 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Kidney transplantation is the optimal treatment for end-stage renal disease, yet long-term graft survival remains limited by allograft rejection. While T and B cells and donor-specific antibodies (DSA) have been the main focus, accumulating evidence indicates that natural killer (NK) cells play a significant dual role in both graft injury and immune adaptation, including in DSA-negative rejection. This narrative review summarizes current knowledge on the dual role of NK cells in kidney transplantation, with emphasis on antibody-independent mechanisms, adaptive NK-cell subsets, and their potential as biomarkers of graft outcome. NK cells are highly heterogeneous, consisting of CD56bright and CD56dimCD16 subsets. Cytomegalovirus infection promotes expansion of adaptive NKG2C+CD57+ cells with memory-like features. In rejection, NK cells act through both antibody-dependent cellular cytotoxicity and antibody-inde-pendent pathways, such as “missing-self” recognition via killer immunoglobulin-like receptors (KIR)/human leukocyte antigen (HLA) mismatch and release of the killer-specific secretory protein of 37 kDa (Ksp37). Specific NK subsets are associated with microvascular inflammation and graft loss even in the absence of DSA. In contrast, NK cells support tolerance by killing donor dendritic cells and activated T cells, producing interleukin (IL)-10 and transforming growth factor-β (TGF-β), and undergoing reeducation, gradually shifting from a cytotoxic to a regulatory phenotype. NK cells exert a dual, often opposing role in kidney transplantation, mediating both allograft injury and immune tolerance. Better understanding of their plasticity may enable new biomarkers and NK-targeted therapies to improve long-term graft survival.]]></description>
            <category>ARTICLE</category>
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        <item>
            <title><![CDATA[Soluble CD163 as a Non-Invasive Biomarker in Autoimmune Nephrological and Rheumatological Diseases]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0024</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0024</guid>
            <pubDate>Tue, 01 Sep 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Autoimmune nephrological and rheumatological diseases involve macrophage-driven inflammation, yet disease activity is often assessed using invasive or non-specific measures. Soluble CD163 (sCD163), released from activated monocytes and macrophages, is emerging as a biomarker of macrophage-mediated inflammation in these conditions. This narrative review summarizes current evidence on the diagnostic, prognostic, and disease-monitoring potential of sCD163 measured in blood, urine, and synovial fluid in autoimmune nephrological and rheumatological diseases. This review is based on a narrative analysis of selected publications investigating the clinical utility of sCD163 in autoimmune kidney and rheumatic diseases, with emphasis on correlations with disease activity, histopathological findings, and clinical outcomes. Urinary sCD163 shows excellent diagnostic accuracy for active lupus nephritis (area under the receiver operating characteristic [AUROC] 0.89–0.998), correlates with histological activity index (but not chronicity), and distinguishes ongoing inflammation from chronic damage during treatment. In IgA nephropathy, it predicts remission failure and greater benefit from corticosteroids. In ANCA-associated vasculitis, it identifies active renal involvement (AUROC 0.95 in multicenter cohorts). In rheumatoid arthritis (RA), serum sCD163 correlates with early disease activity, predicts radiographic progression, and detects subclinical macrophage activation in remission. In spondylarthritis, synovial fluid sCD163 reflects a disease-specific M2-polarized macrophage phenotype distinct from RA. Utility is compartmentalized: urinary levels indicate intrarenal macrophage activation, synovial fluid local joint inflammation, and serum systemic activation. sCD163 is a promising macrophage-specific biomarker across autoimmune diseases, but its compartmentalized nature requires context-specific measurement. Before clinical implementation, assay standardization, multicenter validation, and interventional trials showing the benefit of sCD163-guided management are needed.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Nimbolide Reduces Inflammation and Oxidative Stress to Inhibit Disease Progression in Septic Acute Kidney Injury Mice]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0023</link>
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            <pubDate>Sat, 22 Aug 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[The study investigates the protective role of Nimbolide, a natural limonoid, against sepsis-associated acute kidney injury (SA-AKI) and its underlying molecular mechanisms. A murine sepsis model was established via cecal ligation and perforation. Renal histopathological changes were evaluated by hematoxylin and eosin staining, and renal function was assessed based on serum creatinine (Scr) and blood urea nitrogen (BUN) levels. The levels of inflammatory cytokines (interleukin-6 [IL-6], interleukin-1β [IL-1β], tumor necrosis factor-α [TNF-α]) in serum and renal homogenates were quantified by ELISA. Oxidative stress markers (malondialdehyde [MDA], superoxide dismutase [SOD], glutathione [GSH]) in renal tissue were measured using commercial assay kits. Renal cell apoptosis was detected by transferase dUTP nick end labeling (TUNEL) assay. Also, the protein expression and phosphorylation levels of nuclear factor kappa B (NF-κB) p65 and STAT3 in renal tissues were analyzed by Western blotting. Nimbolide treatment markedly attenuated tubular vacuolization and inflammatory cell infiltration, and improved renal function, as demonstrated by reduced serum Scr and BUN levels. Nimbolide also suppressed the levels of the pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) in both serum and renal tissue. Furthermore, Nimbolide decreased MDA levels, increased SOD activity and GSH content, and inhibited renal apoptosis. Mechanistically, these protective effects were associated with the inhibition of NF-κB p65 and STAT3 phosphorylation in the kidneys. Nimbolide protects against SA-AKI by inhibiting activation of the NF-κB/STAT3 pathway, thereby attenuating inflammation, oxidative stress, and apoptosis.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[sEV-Enriched Serum Preparations From Healthy Individuals Protect Against Acute Pancreatitis-Induced Intestinal Barrier Dysfunction Through miR-579-3p/ANXA3-Mediated Inhibition of NLRP3 Inflammasome Pyroptosis (DOI: 10.2478/aite-2026-0018)]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0022</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0022</guid>
            <pubDate>Thu, 06 Aug 2026 00:00:00 GMT</pubDate>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Isovitexin can Alleviate Fracture-Related Infection, Promote Osteogenesis, and Inhibit Activation of the NF-κB Signaling Pathway]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0021</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0021</guid>
            <pubDate>Mon, 13 Jul 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Fracture-related infection is a challenging aspect of orthopedic care, as it leads to prolonged inflammation and impaired bone healing. Although isovitexin is a naturally occurring flavonoid with anti-inflammatory properties, its effects on fracture-related infection remain unclear. A rat fracture infection model was established and randomly divided into four groups: control, model, Vancomycin, and isovitexin. Tissue staining was used to assess bone healing. In contrast, enzyme-linked immunosorbent assay and biochemical kits were used to measure the levels of inflammatory factors and bone metabolism-related indicators. The expression of proteins associated with osteogenesis and the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway was examined using Western blot. When compared to the model group, isovitexin treatment more effectively reduced inflammatory cell infiltration in bone tissue and promoted callus formation than the Vancomycin group. In addition, isovitexin improved the imbalance of bone metabolism and promoted the expression of osteogenesis-related proteins Bone Morphogenetic Protein 2 (BMP2), Osteopontin (OPN), and Runt-related Transcription Factor 2 (RUNX2). It also decreased the levels of pro-inflammatory factors tumor necrosis factor (TNF)-α and interleukin (IL)-6, and increased the level of the anti-inflammatory factor IL-10. Mechanistic studies showed that isovitexin significantly inhibited the activation of the NF-κB signaling pathway. Isovitexin can promote bone metabolism and healing, suppress the NF-κB signaling pathway, and reduce the inflammatory response associated with fracture-related infection. This study suggests that isovitexin may be a viable therapy option for fracture-related infections.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Heteronemin, a Scalarane Sesterterpenoid, Activates Apoptosis and Non-Apoptotic Ferroptosis and Inhibits Cytoprotective Autophagy in Oral Cancer Cells]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0016</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0016</guid>
            <pubDate>Sat, 04 Jul 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Oral squamous cell carcinoma (OSCC) ranks 16th worldwide as the most common type of malignancy in head and neck cancer globally, and addressing it has been an ongoing but difficult pursuit, as treatment resistance is commonly reported. Hence, employing multiple cell death pathways is an emerging strategy in overcoming treatment resistance in OSCC. We investigate here the effect of heteronemin, a marine sesterterpenoid isolated from sponges, for its anti-cancer potential, hypothesizing that it can induce non-apoptotic cell death pathways to overcome apoptosis-resistant cells and elucidate the underlying mechanisms involved. Our results show that heteronemin significantly kills cancer cells via the induction of the intrinsic apoptotic pathway. It also triggers ferroptosis, down-regulating glutathione peroxidase 4 (GPX4) and upregulating markers of lipid peroxidation such as 4-hydroxynonenal and malondialdehyde. We demonstrate that increasing reactive oxygen species generation plays a central role in triggering these pathways. ensuring the death of the cancer cells despite a compensation attempt via inducing autophagy and modulating Nrf2. Our study is the first to demonstrate the complex but interesting role of heteronemin in killing OSCC cells: inducing apoptosis and switching to ferroptosis as the cells attempt to survive. It also inhibits protective autophagy, leaving OSCC cells incapable of protecting themselves from imminent death. This complex mechanism adds to the existing knowledge on the mechanism of heteronemin as a strong therapeutic compound to treat OSCC cells.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[sEV-Enriched Serum Preparations From Healthy Individuals Protect Against Acute Pancreatitis-Induced Intestinal Barrier Dysfunction Through miR-579-3p/ANXA3-Mediated Inhibition of NLRP3 Inflammasome Pyroptosis]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0018</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0018</guid>
            <pubDate>Thu, 25 Jun 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Acute pancreatitis (AP) frequently triggers intestinal barrier dysfunction, yet the underlying molecular mechanisms remain poorly understood. This study investigated whether small extracellular vesicle (sEV)-enriched serum preparations from healthy individuals protect against AP-induced intestinal barrier dysfunction through microRNA-mediated regulation of pyroptosis. sEV-enriched preparations were isolated from 10 AP patients (AP-sEV) and 10 healthy controls (HC-sEV) using ExoQuick precipitation followed by ultracentrifugation. A murine AP model was established using cerulein and lipopolysaccharide, and human intestinal epithelial cells were stimulated with lipopolysaccharide for in vitro studies. HC-sEV preparations significantly ameliorated AP-induced tissue damage, restored tight junction proteins (claudin-1, occludin, ZO-1), reduced intestinal permeability, and suppressed inflammatory cytokines (TNF-α, IL-6, IL-1β) and pyroptosis-related proteins including NLRP3, gasdermin D, and cleaved caspase-1. Conversely, AP-sEV preparations exacerbated barrier dysfunction. Bioinformatics analysis identified miR-579-3p as significantly downregulated in AP-sEV. Inhibition of miR-579-3p reversed HC-sEV protective effects. ANXA3 was validated as a direct miR-579-3p target, and ANXA3 overexpression counteracted miR-579-3p-mediated protection. These findings demonstrate that HC-sEV preparations protect against AP-induced intestinal barrier dysfunction through miR-579-3p delivery targeting ANXA3 to suppress NLRP3 inflammasome-mediated pyroptosis. The miR-579-3p/ANXA3/NLRP3 axis represents a novel therapeutic target for preserving intestinal barrier integrity during acute pancreatitis.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[NCR1 and NCR3 Expression and Genetic Polymorphism are Associated with CMV Infection after Allogeneic Haematopoietic Stem Cell Transplantation]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0019</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0019</guid>
            <pubDate>Thu, 25 Jun 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Cytomegalovirus (CMV) infection remains a significant cause of morbidity and mortality due to the compromised immune system after hematopoietic stem cell transplantation (HSCT). Natural killer (NK) cells are pivotal in the immune response following HSCT, as these cells regenerate early and play a crucial role in detecting and eliminating infections. In the present study, we analyzed expression and single nucleotide polymorphisms (SNPs) of genes coding for NK cell Natural Cytotoxicity Receptors (NCRs). Expression was studied on the mRNA level and on the protein level, using flow cytometry to examine NCR-positive NK cell populations. Our study revealed significant higher expression of NCR1 and NCR3 in HSCT recipients with CMV infection compared to those without complications. Additionally, expression of both receptors correlated with expression of IFN-γ. Changes over time after HSCT were observed in the proportion of NCR1+ NK cells. SNPs genotyping identified associations of NCR1 rs1433097 and NCR3 rs11575836 genotypes with increased risk of CMV infection, as well as of NCR3 rs11575836 with post-HSCT overall survival. These results underscore the crucial role of NCRs in the prevention of infection and the development of post-HSCT complications, highlighting their potential as therapeutic targets to improve transplant outcomes.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[USP25 Promotes Glycolysis of Acute Myeloid Leukemia Cells and Enhances Tumor Immunity]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0020</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0020</guid>
            <pubDate>Thu, 25 Jun 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Acute myeloid leukemia (AML) is an incursionary hematopoietic tumor with frequent relapses and an unfavorable prognosis. Ubiquitin-specific peptidase 25 (USP25) mediates the progression of various cancers, but its role in AML remains uncharted. The expression of USP25 in AML was analyzed in silico, in vitro, and in vivo through real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. The function of USP25 in proliferation, apoptosis, glycolysis, and immunity in AML was addressed through cell counting kit-8 (CCK-8), flow cytometry, detection of glucose consumption, lactate production, extracellular acidification rate (ECAR), and oxygen consumption rate (OCR), immunohistochemistry, immunofluorescence, and Western blot. The mechanism of USP25 in AML was explored via co-immunoprecipitation (Co-IP), ubiquitination, cycloheximide, and Western blot. Upregulation of USP25 indicated a poor overall survival in AML patients. Knock-in and knock-down results revealed that USP25 enhanced viability, the level of glucose consumption, lactate production, ECAR, and the level of anti-glucose transporter type 1 (GLUT1) and hexokinase-2 (HK2), but reduced the apoptosis rate and the OCR level. Mechanically, USP25 directly bound and deubiquitinated c-Myc. An upregulation of c-Myc and programmed cell death ligand 1 (PD-L1) was found in AML. Knockdown of c-Myc decreased USP25-induced cell viability, glucose consumption, and lactate production level. In vivo, knockdown of USP25 decreased tumor volume and weight, the ki-67 expression, and the levels of c-Myc and PD-L1, but elevated the levels of cluster of differentiation 4 (CD4) and cluster of differentiation 8 (CD8). USP25 facilitated proliferation, glycolysis, and immunity through deubiquitinating c-Myc in AML. The results identified USP25 as a possible target for AML treatment.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Herd-Trained Immunity: A Hidden Component of Population-Level Innate Immunity]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0017</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0017</guid>
            <pubDate>Mon, 22 Jun 2026 00:00:00 GMT</pubDate>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Saccharomyces cerevisiae β-Glucan Training Induces a Nonclassical PGE2−High/NO−Low Macrophage Phenotype in Response to Pseudomonas aeruginosa Exopolysaccharide]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0014</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0014</guid>
            <pubDate>Sun, 31 May 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Exopolysaccharide (EPS), a major constituent of Pseudomonas aeruginosa biofilms, protects bacteria from M1-macrophage-mediated clearance while promoting chronic inflammation. This study investigated how Saccharomyces cerevisiae β-glucan (BG)-induced macrophage training reshapes subsequent inflammatory and antimicrobial responses to EPS. Peritoneal macrophages from C57BL/6 mice were trained in vitro with BG and subsequently stimulated with EPS purified from a clinical P. aeruginosa isolate obtained from a patient with severe cystic fibrosis. Cytokines, prostaglandin E2 (PGE2), and nitric oxide (NO) were quantified, and global proteomic profiling was performed. BG training amplified EPS-induced secretion of TNF-α, IL-6, and additional pro-inflammatory mediators. Trained macrophages also showed markedly increased PGE2 production, minimal NO release, and reduced phagocytic activity. Proteomic analyzes confirmed upregulation of PGE2-biosynthetic enzymes and suppression of inducible NO synthase, along with enhanced expression of antimicrobial and immunoregulatory factors, including platelet factor 4, antileucoproteinase, C1q components, and selected chemokines. These data reveal a previously uncharacterized macrophage state—neither M1 nor M2—emerging specifically from BG training and defined by high PGE2 and low NO production in response to EPS. S. cerevisiae BG training reprograms EPS-stimulated macrophages toward a distinct, non-classical trained-immunity phenotype characterized by elevated PGE2 and suppressed NO production. This newly defined phenotype represents a novel form of trained immunity and highlights the dual proinflammatory and immunoregulatory roles of macrophage-derived PGE2. These findings suggest that targeted macrophage reprogramming may offer a promising therapeutic strategy for mitigating P. aeruginosa biofilm-driven chronic inflammation, including in cystic fibrosis.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Salvianolic Acid C Activates the AMPK Pathway to Inhibit Ferroptosis and Alleviate Cardiomyocyte Injury after Acute Myocardial Infarction]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0015</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0015</guid>
            <pubDate>Sat, 16 May 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Myocardial infarction (MI) is one of the leading causes of death worldwide and results in substantial harm to human health and family well-being. Salvianolic acid C (SAC), a bioactive compound isolated from Salvia miltiorrhiza Bge., exhibits anti-oxidant, anti-inflammatory, and anti-apoptotic capacities. However, the protective effects of SAC against MI-induced cardiomyocyte injury and the underlying molecular mechanisms, particularly its role in ferroptosis and AMPK signaling, remain unclear. Infarct size in rat hearts was assessed through triphenyltetrazolium chloride (TTC) staining. Myocardial tissue damage was examined through hematoxylin-eosin (HE) staining. The mRNA and protein levels of inflammatory cytokines, including Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, were measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Apoptosis in myocardial tissues was evaluated through the terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL) assay. Protein expression levels were determined by Western blot. The results demonstrated that SAC significantly reduced infarct size in MI rats. Inflammation and cardiomyocyte apoptosis were markedly increased in the MI group, but these impacts were neutralized after SAC treatment. In addition, SAC effectively suppressed ferroptosis in MI rats. Mechanistically, SAC activates the AMPK pathway. Finally, SAC was shown to alleviate oxygen-glucose deprivation (OGD)-induced cardiomyocyte injury by activating the AMPK pathway. This study is the first to demonstrate that SAC activates the AMPK pathway to inhibit ferroptosis and alleviate cardiomyocyte injury after acute MI. These findings suggest that SAC may present a promising therapeutic candidate for the treatment of MI.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[BDH2 Inhibits Lung Adenocarcinoma Metastasis by Promoting Ferroptosis]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0012</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0012</guid>
            <pubDate>Thu, 09 Apr 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[To investigate the role of 3-hydroxybutyrate dehydrogenase 2 (BDH2) in regulating ferroptosis and its impact on the metastasis of lung adenocarcinoma (LUAD). Expression levels of BDH2 were modulated in LUAD cell lines (A549, PC9) using pcDNA-BDH2 plasmid transfection. Cell motility was assessed by Transwell assays, while ferroptosis-associated markers, including Fe2+, malondialdehyde (MDA), lipid reactive oxygen species (ROS), ACSL4, and GPX4, were evaluated by biochemical assays, flow cytometry, and Western blotting. The involvement of the Nrf2/HO-1 signaling axis was analyzed by Western blotting and RT-qPCR. Furthermore, a xenograft mouse model was established to confirm the effect of BDH2 on tumor progression and metastasis in vivo. Overexpression of BDH2 significantly inhibited LUAD cell migration and invasion. BDH2 upregulation enhanced ferroptosis, effects that were reversed by the ferroptosis inhibitor Fer-1. Mechanistically, BDH2 suppressed the activation of the Nrf2/HO-1 pathway, thereby enhancing sensitivity to ferroptosis. In vivo, BDH2 overexpression markedly reduced tumor growth and metastasis in nude mice, while inhibition of ferroptosis attenuated these effects. BDH2 suppresses metastasis in LAUD by promoting ferroptosis via suppression of the Nrf2/HO-1 pathway, highlighting BDH2 as a potential therapeutic target for LUAD.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Di-Chimeric Cell Therapy Derived From Hematopoietic and Mesenchymal Stem Cells Promotes Immune Tolerance and Extends Vascularized Composite Allograft Survival]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0013</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0013</guid>
            <pubDate>Thu, 09 Apr 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Chimerism-based strategies remain promising for tolerance induction in solid organ and vascularized composite allograft (VCA) transplantation. This study aimed to develop a novel, less toxic chimeric cell therapy to prolong allograft survival and reduce the need for lifelong immunosuppression. Di-chimeric cells (DCC) were created via polyethylene glycol (PEG)-mediated ex vivo fusion of allogeneic hematopoietic stem cells (HSC) and mesenchymal stem cells (MSC) derived from August Copenhagen Irish (ACI) and Lewis rats. Twenty-four fully major histocompatibility complex (MHC)-mismatched groin flap VCAs were transplanted from ACI rat major histocompatibility complex (rat MHC) (RT1a) donors to Lewis (RT11) recipients under a 7-day immunosuppressive protocol of anti-αβTCR antibody and tacrolimus, combined with four different cell therapies of n = 6/group: Group 1, saline control; Group 2, MSC; Group 3, HSC/HSC DCC; and Group 4, HSC/MSC DCC. DCC were delivered via the intraosseous injection. DCC phenotype was confirmed by flow cytometry (FC). Graft rejection was evaluated macroscopically. A single DCC dose significantly prolonged VCA survival, with the best results in Group 4 (94 ± 1.65 days), followed by Group 3 (66 ± 1.24 days), Group 2 (45.5 ± 4.08 days), and Group 1 (38 ± 4.29 days). This study confirmed immunomodulatory and tolerogenic properties of DCC, supporting VCA transplantation.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Fusobacterium nucleatum Promotes Bladder Cancer Development Through lncRNA IDH1-AS1-Mediated Autophagy]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0011</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0011</guid>
            <pubDate>Tue, 31 Mar 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Bladder cancer is a prevalent malignancy with a high recurrence rate, necessitating the identification of novel molecular targets for diagnosis and therapy. Recent studies have highlighted the role of long noncoding RNAs (lncRNAs) in cancer progression. This study aims to investigate the role of the lncRNA IDH1-AS1 in bladder cancer, focusing on its effects on tumor growth, cell proliferation, and autophagy-related protein expression. We utilized both in vivo and in vitro models to assess the impact of IDH1-AS1 overexpression and knockdown. Tumor growth was evaluated in nude mice model of bladder cancer, while cell proliferation was measured using the EDU assay. Protein expression levels of Beclin1, P62, and LC3 were determined by Western Blot analysis. Gene expression of IDH1-AS1 was quantified using quantitative polymerase chain reaction (qPCR). Overexpression of IDH1-AS1 in nude mice model of bladder cancer led to a significant increase in tumor volume and weight, whereas knockdown of IDH1-AS1 resulted in a substantial decrease in tumor size. In vitro, IDH1-AS1 overexpression significantly enhanced cell proliferation, while its knockdown reduced proliferation. Western Blot analysis revealed that IDH1-AS1 overexpression increased the levels of autophagy-related proteins Beclin1 and LC3, and decreased P62 protein levels, with contrary effects observed upon IDH1-AS1 knockdown. qPCR confirmed successful modulation of IDH1-AS1 expression in experimental groups. Our findings indicate that IDH1-AS1 promotes tumor growth and cell proliferation in bladder cancer, potentially through the regulation of autophagy-related proteins. These results suggest that IDH1-AS1 could serve as a novel biomarker and therapeutic target for bladder cancer.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Bowel-Associated Dermatosis and Arthritis Syndrome (BADAS) – A Literature Review With Diagnostic and Therapeutic Implications and a Report of Two Cases of BADAS Associated With Inflammatory Bowel Disease]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0010</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0010</guid>
            <pubDate>Sat, 21 Feb 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Bowel-associated dermatosis–arthritis syndrome (BADAS) is a rare neutrophilic dermatosis characterized by recurrent erythematous macules, papules or vesicopustules accompanied by fever, malaise, arthralgia and peripheral arthritis. Although originally described after intestinal bypass procedures, BA-DAS is increasingly recognized in inflammatory bowel disease (IBD), yet remains underdiagnosed and lacks practical guidance. We reviewed published IBD-associated BADAS cases to define clinical patterns and therapeutic options, and report two additional cases managed by an interdisciplinary team. Across the literature, 21 IBD-associated BADAS cases were identified, with a female predominance (65%) and a mean age at onset of 36.7 years; pediatric presentations accounted for 17%. Ulcerative colitis (12 cases) and Crohn’s disease (10 cases) were the most frequent underlying conditions. BADAS was often diagnosed concurrently with IBD, indicating that the combination of cutaneous eruptions, joint inflammation and systemic symptoms should prompt gastrointestinal evaluation. Frequently reported abnormalities included leukocytosis, anemia and elevated inflammatory markers, and skin histopathology typically showed a neutrophilic dermatosis often with leukocytoclastic vasculitis. Case 1 (30-year-old woman with ulcerative colitis) achieved sustained remission with antibiotics, corticosteroid taper, cyclosporine induction and azathioprine maintenance. Case 2 (67-year-old man with Crohn’s disease) responded to antibiotics followed by infliximab, with resolution of skin, joint and intestinal activity. We propose a pragmatic management approach integrating antibiotics, optimization of IBD therapy and early use of biologics (preferably anti-TNF) in severe or steroid-refractory disease.]]></description>
            <category>ARTICLE</category>
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        <item>
            <title><![CDATA[Mechanism of RBM15 in Regulating PD-L1-Mediated Immune Escape in Ovarian Cancer Through the JAK2/STAT3/STAT5 Pathway]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0009</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0009</guid>
            <pubDate>Wed, 11 Feb 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[This paper elucidates the role of RNA-binding motif protein 15 (RBM15) in programmed death-ligand 1 (PD-L1)-mediated immune escape in ovarian cancer (OC), providing a novel immunotherapeutic strategy. RBM15/circFGFR3/JAK2/STAT3/STAT5 expression was assessed. OC cell progression was analyzed. OC cells were co-cultured with CD8+ T cells. The m6A enrichment on circRNA fibroblast growth factor receptor 3 (circFGFR3) was determined. The expression of p-JAK2, p-STAT3, and p-STAT5 was investigated. The bindings of circFGFR3 to EIF4A3 and EIF4A3 to JAK2, STAT3, or STAT5 were analyzed. In conclusion, RBM15 promotes PD-L1-mediated immune escape and accelerates OC progression by upregulating circFGFR3 expression through m6A modification and activating the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway.]]></description>
            <category>ARTICLE</category>
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        <item>
            <title><![CDATA[Neuronal Transdifferentiation in Humans: Protocols for Monocytes Conversion into Neuronal-Like Cells with Small Molecules]]></title>
            <link>https://reference-global.com/article/10.2478/aite-2026-0008</link>
            <guid isPermaLink="false">/article/10.2478/aite-2026-0008</guid>
            <pubDate>Mon, 26 Jan 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Neurodegenerative diseases, such as Parkinson's, Alzheimer's, and Huntington's, are major causes of disability. Current treatments are mostly symptomatic, due to a limited understanding of the disease mechanisms and the brain's poor regenerative capacity. Neuronal transdifferentiation offers a promising solution. Existing protocols are often inefficient, invasive, or time-consuming, and expensive. Furthermore, they mostly rely on nucleic acids as transdifferentiation-inducers, hence this carries risks of insertion mutagenesis. In this study, monocytes were isolated from buffy coats and cultured under four protocols using different small-molecule combinations. Two protocols successfully generated TUJ1+ MAP2+ SYP+ cells. Transdifferentiation is achievable through cheap and efficient chemical induction.]]></description>
            <category>ARTICLE</category>
        </item>
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