Role of Heat Shock Proteins in Climate-Induced Cardiovascular Damage

Heat shock proteins (HSPs) are a highly conserved family of proteins that are rapidly produced in response to cellular stress, particularly elevated temperatures. They play a critical role in maintaining cellular integrity by stabilizing, repairing, and refolding damaged proteins. First identified in Drosophila melanogaster, HSPs are induced even by mild thermal stress and have been shown to protect a variety of tissues, including the heart and vasculature. While previous reviews have largely focused on general stress responses and cardiovascular physiology, the effects of climate-related stressors—such as heat waves, extreme temperatures, and environmental heat exposure-on cardiovascular health via HSP activation remain underexplored. This review examines the emerging evidence on HSP-mediated cardiovascular protection under climate-induced stress. We highlight how HSPs support cardiomyocyte survival, maintain calcium homeostasis, preserve electrical stability, and enhance ischemic tolerance. Their roles in protecting vascular compartments, preventing hypertrophy, atherosclerosis, obesity-related dysfunction, and limiting metabolic, oxidative, and inflammatory injury are also discussed. By integrating these findings, we illustrate the multifaceted ways in which HSPs mitigate cardiovascular risks associated with rising global temperatures. Understanding the interplay between environmental stressors and HSP biology is increasingly important in a warming world. HSPs not only act as intrinsic cellular defense mechanisms but also represent promising therapeutic targets for enhancing cardiovascular resilience. By bridging molecular mechanisms with clinical implications, this review addresses critical gaps in the literature and provides a comprehensive perspective on how HSPs can help protect cardiovascular health in the face of climate change.