Abstract
Small heat shock protein 22 (HSP22) belongs to the superfamily of heat shock proteins and is predominantly expressed in the heart, brain, skeletal muscle, and different types of cancers. It has been found that HSP22 is involved in variant cellular functions in cardiomyocytes and plays a vital role in cardiac protection against cardiomyocyte injury under diverse stress. This review summarizes the multiple functions of HSP22 in the heart and the underlying molecular mechanisms through modulating gene transcription, post-translational modification, subcellular translocation of its interacting proteins, and protein degradation, facilitating mitochondrial function, cardiac metabolism, autophagy, and ROS production and antiapoptotic effect. We also discuss the association of HSP22 in cardiac pathologies, including human dilated cardiomyopathy, pressure overload-induced heart failure, ischemic heart diseases, and aging-related cardiac metabolism disorder. The collected information would provide insights into the understanding of the HSP22 in heart diseases and lead to discovering the therapeutic targets.
Highlights
The heat shock proteins (HSPs) are a family of proteins that have been linked to different cellular functions in multiple tissues
We focus on the studies of multiple functions of heat shock protein 22 (HSP22) in the heart, outlining the associated molecular mechanisms involved in cytoprotection of cardiomyocytes, and its modulation in autophagy, mitochondrial function, energy metabolism, and oxidative stress
Deleting the N-terminal domain of HSP22 blocks its mitochondrial translocation, attenuates inducible nitric oxide synthase (iNOS) mitochondrial distribution, and subsequently impairs oxidative phosphorylation, preventing cytoprotection [35]. These findings are important since cardioprotection by NO donors has been limited so far; the observed protective effects of iNOS induced by HSP22 imply that stimulating endogenous iNOS mitochondrial translocation inside the cardiac myocytes might have better biological efficiency than that provided by NO donors
Summary
The heat shock proteins (HSPs) are a family of proteins that have been linked to different cellular functions in multiple tissues. Previous studies showed that HSP22 is predominately expressed in a limited number of tissues under physiological conditions, including heart and skeletal muscle, and is involved in the regulation of cell growth, leading to cardiac hypertrophy [6,16]. It has been shown that overexpression of HSP22 protects cardiomyocytes against oxidative stress-induced cell death in vitro and reduces myocardial ischemic injury in vivo [20–23]. Another recent study showed that HSP22 suppresses diabetes-induced endothelial injury [24]. One more recent study showed that the loss of HSP22 progressively induced cardiac dilation and dysfunction [26] All these studies have highlighted the importance of HSP22 in the heart under both physiological and pathological conditions. It would bring a fresh perspective into understanding the role of HSP22 in other conditions, such as cancers, neurological disorders, and age-related diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
