What is it about?
Protein kinases are important signalling molecules which have been shown to have important roles during heart disease. This study provides experimental evidence for a role of p38 gamma mitogen-activated protein kinase (p38gamma MAPK) in the progression of cardiac hypertrophy and heart failure and describes a plausible mechanism of action. The study uses a mouse model of cardiac hypertrophy and heart failure and the study demonstrates how knocking out the gene for of p38gamma MAPK preserves cardiac function following a surgical procedure that causes mice to develop heart failure. Then using a modified kinase molecule in vitro and subsequent biochemical analysis we have identified three downstream substrates (signalling partners) of p38gamma MAPK and demonstrate the functional consequence of substrate activation. This provides new insights in to the function of this protein kinase in heart disease and possible therapeutic targets.
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Why is it important?
This work shows that the kinase p38 gamma in responsible for remodelling of the heart following pressure overload caused by hypertension and acts through the interacting with the protein calpastatin which controls the activity of the enzyme calpain.
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This page is a summary of: p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin, The FASEB Journal, October 2019, Federation of American Societies For Experimental Biology (FASEB), DOI: 10.1096/fj.201701545r.
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