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NFAT and Cardiac Hypertrophy

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Description

Cardiac failure, one of the largest health care burdens in the United States and other developed countries is often associated with prolonged and maladaptive cardiac hypertrophy, defined as a compensatory mechanism of the heart that helps to maintain cardiac output during pathological states with sustained increases in hemodynamic load (Ref.1). As cardiomyocytes lose the ability to divide soon after birth, cardiac hypertrophy offers an important adaptive response in vivo that allows the organism to maintain or increase its cardiac output. The adult myocardium responds to a wide array of intrinsic and extrinsic stimuli, including hypertension, myocardial infarction, cardiac arrhythmias, valvular disease, endocrine disorders, increased workload, injury, and contractile abnormalities resulting from mutant sarcomeric proteins by hypertrophic growth (Ref.2). Although initially [...]

References:

1.Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes.
Fiedler B, Lohmann SM, Smolenski A, Linnemuller S, Pieske B, Schroder F, Molkentin JD, Drexler H, Wollert KC.
Proc Natl Acad Sci U S A. 2002 Aug 20; 99(17): 11363-8. Epub 2002 Aug 12.
2.Prevention of cardiac hypertrophy by calcineurin inhibition: hope or hype?
Olson EN, Molkentin JD.
Circ Res. 1999 Apr 2; 84(6): 623-32. Review. No abstract available.
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