Heat Shock Protein 90 In Sepsis-Induced Cardiomyopathy: Mechanistic Insights And Emerging Therapeutic Target

Sepsis-induced cardiomyopathy (SIC) is a form of cardiac dysfunction triggered by sepsis, whose pathogenesis primarily involves the release of endogenous danger signal molecules. As a key molecular chaperone, Heat Shock Protein 90 (Hsp90) plays a fundamental role in stabilizing and activating client proteins to regulate essential cellular processes. Although the broader heat shock protein family has been studied in SIC, the specific mechanisms and therapeutic potential of Hsp90 remain to be fully elucidated. Hsp90 plays a crucial role in apoptosis, oxidative stress, mitochondrial autophagy, immune defense, and myocardial fibroblast function during heart dysfunction. This review systematically summarizes the structure and regulatory mechanisms of Hsp90 in SIC. Furthermore, we discuss recent advances in Hsp90 inhibitors which was categorized natural product-derived inhibitors, functional inhibitors, and structural disruptors, thereby providing a theoretical foundation and prospective strategies for novel therapeutic interventions against SIC.