Abstract
Introduction Small heat shock proteins (sHSPs) are a family of molecular chaperones which play an important role in mitigating and preventing the aggregation of misfolded proteins under conditions of stress such as hypoxia or heat and thereby contribute to maintaining intracellular homeostasis. These properties are exploited in many organs, including the heart where they are thought to play a crucial role in the cardiac hypertrophy. Cardiac hypertrophy is a condition in which the heart compensates for a pressure overload caused by several cardiovascular diseases. However, cardiac hypertrophy itself poses a health risk as it increases the risk of severe cardiovascular events. Clarifying the role of sHSPs in normal as well as hypertrophic condition could be important in understanding the underlying mechanism of sHSPs in heart functioning.
Objective To evaluate the role small heat shock proteins in the pathogenesis of cardiac hypertrophy.
Method The literature was searched using biomedical databases MEDLINE and Embase for studies that did research into small heat shock proteins focusing on their role in the development of hypertrophy in cardiac cells.
Results HspB5 possibly exerts its cardioprotection by suppressing the NFAT signaling pathway. Overexpression of HspB5 protects against transoartic constriction (TAC) induced
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These stresses cause a pressure overload which induce changes in myocardial structure and function. This initially acts a compensatory mechanism but when pressure overload persists it can lead to the development of cardiac hypertrophy (Lyon et al., Mechanotransduction in Cardiac Hypertrophy and Failure) . Cardiac hypertrophy is strongly associated with in an increased risk of several severe cardiovascular events, including stroke, coronary heart disease and heart failure (Gosse,