Regulation of Sam68 activity by small heat shock protein 22

2006 ◽  
Vol 99 (5) ◽  
pp. 1353-1362 ◽  
Author(s):  
Kameswara R. Badri ◽  
Suhasini Modem ◽  
Herve C. Gerard ◽  
Insia Khan ◽  
Mihir Bagchi ◽  
...  
Cells ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 114
Author(s):  
Xiaonan Sun ◽  
Sharadhi Siri ◽  
Amirah Hurst ◽  
Hongyu Qiu

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.


Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1550
Author(s):  
Wenqian Wu ◽  
Xiaonan Sun ◽  
Xiaomeng Shi ◽  
Lo Lai ◽  
Charles Wang ◽  
...  

Heat shock protein 22 (Hsp22) is a small heat shock protein predominantly expressed in skeletal and cardiac muscle. Previous studies indicate that Hsp22 plays a vital role in protecting the heart against cardiac stress. However, the essential role of Hsp22 in the heart under physiological conditions remains largely unknown. In this study, we used an Hsp22 knockout (KO) mouse model to determine whether loss of Hsp22 impairs cardiac growth and function with increasing age under physiological conditions. Cardiac structural and functional alterations at baseline were measured using echocardiography and invasive catheterization in Hsp22 KO mice during aging transition compared to their age-matched wild-type (WT) littermates. Our results showed that Hsp22 deletion induced progressive cardiac dilation along with declined function during the aging transition. Mechanistically, the loss of Hsp22 impaired BCL-2–associated athanogene 3 (BAG3) expression and its associated cardiac autophagy, undermined cardiac energy metabolism homeostasis and increased oxidative damage. This study showed that Hsp22 played an essential role in the non-stressed heart during the early stage of aging, which may bring new insight into understanding the pathogenesis of age-related dilated cardiomyopathy.


2013 ◽  
Vol 23 (8) ◽  
pp. 656-663 ◽  
Author(s):  
Khriezhanuo Nakhro ◽  
Jin-Mo Park ◽  
Ye Jin Kim ◽  
Bo Ram Yoon ◽  
Jeong Hyun Yoo ◽  
...  

2004 ◽  
Vol 36 (6) ◽  
pp. 597-601 ◽  
Author(s):  
Joy Irobi ◽  
Katrien Van Impe ◽  
Pavel Seeman ◽  
Albena Jordanova ◽  
Ines Dierick ◽  
...  

Neurology ◽  
2010 ◽  
Vol 74 (6) ◽  
pp. 502-506 ◽  
Author(s):  
S. J. Kolb ◽  
P. J. Snyder ◽  
E. J. Poi ◽  
E. A. Renard ◽  
A. Bartlett ◽  
...  

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