P62 Stages an Interplay Between the Ubiquitin-Proteasome System and Autophagy in the Heart of Defense Against Proteotoxic Stress

Huabo Su; Xuejun Wang

doi:10.1016/j.tcm.2012.05.015

P62 Stages an Interplay Between the Ubiquitin-Proteasome System and Autophagy in the Heart of Defense Against Proteotoxic Stress

Huabo Su, Xuejun Wang

Research output: Contribution to journal › Review article › peer-review

71 Scopus citations

Abstract

As exemplified by desmin-related cardiomyopathy and myocardial ischemia/reperfusion injury, proteasome functional insufficiency plays an essential pathogenic role in the progression of cardiac diseases with elevated proteotoxic stress. Upregulation of p62/SQSTM1 and increased selective autophagy in cardiomyocytes may protect against proteotoxic stress in the heart. p62 may serve as a proteotoxic stress sensor, promote segregation and degradation of misfolded proteins by autophagy, and mediate the cross talk between the ubiquitin-proteasome system and autophagy.

Original language	English (US)
Pages (from-to)	224-228
Number of pages	5
Journal	Trends in Cardiovascular Medicine
Volume	21
Issue number	8
DOIs	https://doi.org/10.1016/j.tcm.2012.05.015
State	Published - Nov 2011
Externally published	Yes

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/j.tcm.2012.05.015

Cite this

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title = "P62 Stages an Interplay Between the Ubiquitin-Proteasome System and Autophagy in the Heart of Defense Against Proteotoxic Stress",

abstract = "As exemplified by desmin-related cardiomyopathy and myocardial ischemia/reperfusion injury, proteasome functional insufficiency plays an essential pathogenic role in the progression of cardiac diseases with elevated proteotoxic stress. Upregulation of p62/SQSTM1 and increased selective autophagy in cardiomyocytes may protect against proteotoxic stress in the heart. p62 may serve as a proteotoxic stress sensor, promote segregation and degradation of misfolded proteins by autophagy, and mediate the cross talk between the ubiquitin-proteasome system and autophagy.",

author = "Huabo Su and Xuejun Wang",

note = "Funding Information: We are in debt to the former and current members of our laboratory for their contributions to the work summarized here. Dr. Wang is a recipient of the Established Investigator Award of the American Heart Association. This work is supported in part by National Institutes of Health grants R01HL085629 , R01HL072166 , and R01HL068936 and American Heart Association grants 0740025N (X. W.) and 11SDG6960011 (H.S.).",

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doi = "10.1016/j.tcm.2012.05.015",

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N2 - As exemplified by desmin-related cardiomyopathy and myocardial ischemia/reperfusion injury, proteasome functional insufficiency plays an essential pathogenic role in the progression of cardiac diseases with elevated proteotoxic stress. Upregulation of p62/SQSTM1 and increased selective autophagy in cardiomyocytes may protect against proteotoxic stress in the heart. p62 may serve as a proteotoxic stress sensor, promote segregation and degradation of misfolded proteins by autophagy, and mediate the cross talk between the ubiquitin-proteasome system and autophagy.

AB - As exemplified by desmin-related cardiomyopathy and myocardial ischemia/reperfusion injury, proteasome functional insufficiency plays an essential pathogenic role in the progression of cardiac diseases with elevated proteotoxic stress. Upregulation of p62/SQSTM1 and increased selective autophagy in cardiomyocytes may protect against proteotoxic stress in the heart. p62 may serve as a proteotoxic stress sensor, promote segregation and degradation of misfolded proteins by autophagy, and mediate the cross talk between the ubiquitin-proteasome system and autophagy.

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P62 Stages an Interplay Between the Ubiquitin-Proteasome System and Autophagy in the Heart of Defense Against Proteotoxic Stress

Abstract

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