Does Contractile Ca 2+ Control Calcineurin-NFAT Signaling and Pathological Hypertrophy in Cardiac Myocytes?
Year: 2008
Type: article
Abstract: In noncontractile cells, a sustained increase in total cytoplasmic Ca(2+) concentration is typically needed to activate the intracellular protein phosphatase calcineurin, leading to dephosphorylation of the transcription factor nuclear factor of activated T cells (NFAT), its nuclear translocation, and induction of gene expression. It remains a mystery exactly how Ca(2+)-dependent signaling pathways, such as that mediated by calcineurin-NFAT, are regulated in contracting cardiac myocytes given the highly specialized manner in which Ca(2+) concentration rhythmically cycles in excitation-contraction coupling. Here, we critically review evidence that supports the hypothesis that calcineurin-NFAT signaling is regulated by contractile Ca(2+) transients in cardiac myocytes.
Source: Science Signaling
Authors: Steven R. Houser, Jeffery D. Molkentin
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Awards: G1106861790, Calcium and Cardiac Regeneration after Myocardial Infarction, Mitochondrial Regulated Cardiac Myocyte Death, Signaling Processes Underlying Cardiovascular Function, Molecular pathways controlling cardiac gene expression, Ca2+ Regulation in Newly Formed Ventricular Myocytes, Calcium as a Molecular Signal in the Heart, Genetic and Molecular Signaling in Heart Failure, Molecular Pathways Controlling Cardiac Gene Expression, Cardiac hypertrophic intracellular signaling pathways
OpenAlex ID: W2073595175