Heat Shock Proteins in Cardiovascular Stress

Abstract

Heat shock proteins (HSPs) are primarily induced in response to stress stimuli. In cardiovascular diseases, HSPs are expressed pronouncedly and act to protect the cardiac tissue by inhibition of cellular apoptopic mechanisms. An ischemic condition preceded by angina prevents degeneration of tissue by 'ischemic preconditioning' in which HSPs produced in an earlier response have a protective effect towards subsequent cardiac injuries. This review highlights the manifestations of HSPs upon stress conditions of the cardiovascular system. The distinctive features of different HSP families in view of their unique behavior in maintenance of stressed cardiac tissues are briefl y described. A correlation of the fundamental roles of HSPs in certain cardiac pathological conditions is also discussed. A proteomic approach to study the interactions of HSPs is also documented. Hence, an understanding of the physiological mechanisms of HSPs in cardiac stress offers potential solutions for management of cardiac pathologies and to undertake suitable prophylactic measures.

Heat shock proteins: Biological functions, pathological roles, and therapeutic opportunities

“…HSPs are expressed pronouncedly in CVDs, which play a cardioprotective role by inhibiting apoptosis. 197 Numerous studies have shown that preinduction of HSPs by mild stress has a protective effect on a more severe stress, which is related to the amount of induced HSP. 198 In addition, overexpression of HSPs in cultured cardiomyocytes or transgenic animals or intact hearts using viral vectors also has a protective effect, which directly demonstrates the ability of HSPs to protect cardiac function.…”

“…On the one hand, HSPs are initially induced by stress stimuli. HSPs are expressed pronouncedly in CVDs, which play a cardioprotective role by inhibiting apoptosis 197 . Numerous studies have shown that preinduction of HSPs by mild stress has a protective effect on a more severe stress, which is related to the amount of induced HSP 198 .…”