Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 52, Issue 3, Pages 526-537Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2011.10.023
Keywords
Ubiquitin; Proteasome; JNK; c-Jun; Calcineurin; FOXO; p53; Estrogen receptor; Cardiac hypertrophy; Ischemia; Diabetes
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Funding
- National Institutes of Health [R37HL065619, R01HL104129]
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Awareness of the regulation of cell signaling by post-translational ubiquitination has emerged over the past 2 decades. Like phosphorylation, post-translational modification of proteins with ubiquitin can result in the regulation of numerous cellular functions, for example, the DNA damage response, apoptosis, cell growth, and the innate immune response. In this review, we discuss recently published mechanisms by which the ubiquitin proteasome system regulates key signal transduction pathways in the heart, including MAPK JNK, calcineurin, FOXO, p53, and estrogen receptors a and l. We then explore how ubiquitin proteasome system-specific regulation of these signal transduction pathways plays a role in the pathophysiology of common cardiac diseases, such as cardiac hypertrophy, heart failure, ischemia reperfusion injury, and diabetes. This article is part of a Special Section entitled Post-translational Modification. (C) 2011 Elsevier Ltd. All rights reserved.
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