Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 51, Issue 4, Pages 485-490Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2010.10.021
Keywords
p38 kinase mitogen-activated protein kinase; Heart failure; Inhibitor; Therapy
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Funding
- NHLBI NIH HHS [R01 HL103205, R01 HL062311, R01 HL108186, R01 HL070079, R01 HL062311-09, R01 HL103205-01] Funding Source: Medline
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The p38 mitogen-activated protein kinases (p38s) are stress-activated Ser/Thr kinases. Their activation has been associated with various pathological stressors in the heart. Activated p38 is implicated in a wide spectrum of cardiac pathologies, including hypertrophy, myocardial infarction, as well as systolic and diastolic heart failure. In this review, the specific contribution of different isoforms of p38 kinases to cardiac diseases as well as TAB-1-mediated non-canonical activation pathway are discussed as a rationale for inhibiting p38 activity to treat cardiac hypertrophy, ischemic injury, and heart failure. Finally, a summary of current clinical trials targeting p38 kinases in cardiovascular diseases is provided to highlight the potential promise as well as existing challenges of this therapeutic approach. This article is part of a special issue entitled Key Signaling Molecules in Hypertrophy and Heart Failure. (C) 2010 Elsevier Ltd. All rights reserved.
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