Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011 Oct;51(4):485-90.
doi: 10.1016/j.yjmcc.2010.10.021. Epub 2010 Nov 6.

The p38 mitogen-activated protein kinase pathway--a potential target for intervention in infarction, hypertrophy, and heart failure

Affiliations
Review

The p38 mitogen-activated protein kinase pathway--a potential target for intervention in infarction, hypertrophy, and heart failure

Michael S Marber et al. J Mol Cell Cardiol. 2011 Oct.

Abstract

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."

PubMed Disclaimer

Similar articles

Cited by

References

    1. Eyers PA, van den Ijssel P, Quinlan RA, Goedert M, Cohen P. Use of a drug-resistant mutant of stress-activated protein kinase 2a/p38 to validate the in vivo specificity of SB203580. FEBS Letts. 1999;451:191–6. - PubMed
    1. Rakhit RD, Kabir AN, Mockridge JW, Saurin A, Marber MS. Role of G proteins and modulation of p38 MAPK activation in the protection by nitric oxide against ischemia-reoxygenation injury. Biochem Biophys Res Commun. 2001;286:995–1002. - PubMed
    1. Wang Y, Huang S, Sah VP, Ross J, Brown JH, Han J, et al. Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen activated protein kinase family. J Biol Chem. 1998;273(4):2161–8. - PubMed
    1. Saurin AT, Martin JL, Heads RJ, Foley C, Mockridge JW, Wright MJ, et al. The role of differential activation of p38-mitogen-activated protein kinase in preconditioned ventricular myocytes. FASEB J. 2000;14:2237–46. - PubMed
    1. Schulz R, Gres P, Skyschally A, Duschin A, Belosjorow S, Konietzka I, et al. Ischemic preconditioning preserves connexin 43 phosphorylation during sustained ischemia in pig hearts in vivo. Faseb J. 2003;17:1355–7. - PubMed

MeSH terms

Substances