Year: 2010
Type: review
Abstract: D uring the development of cardiac hypertrophy, heart failure, and ischemia reperfusion challenge, the heart accumulates misfolded proteins as a result of cellular stresses.[1][2][3][4] Although the compensatory increases in chaperones/cochaperones work to prevent misfolding, refold denatured proteins, and/or target them for degradation, this system can become overwhelmed, leading to worsening of cardiac function.In fact, recent studies have demonstrated experimentally that increasing the burden of misfolded proteins in the heart can contribute to the development of cardiac dysfunction.5 In this review, we discuss the role of heat shock proteins (HSPs) in common cardiac diseases, including cardiac hypertrophy, heart failure, and ischemia/reperfusion injury.Furthermore, we delineate the many specific mechanisms by which these chaperones, cochaperones, and heat shock factor (HSF) transcription factors have been found to be cardioprotective in experimental models.Lastly, we review recent studies involving drugs that are being developed (and currently used) to increase the expression (and presumably function) of chaperone/cochaperone systems that may be applicable to the treatment of common cardiac diseases and familial cardiac diseases with a pathogenesis that includes a major component of misfolded proteins (eg, desminopathies).
Source: Circulation
Authors: Monte S. Willis, Cam Patterson
Institution: University of North Carolina at Chapel Hill
Language: English
Topic: Heat shock proteins research
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2100810063