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Cardiac Hypertrophy: Signal Transduction, Transcriptional Adaptation, and Altered Growth Control
Author(s) -
WAGNER MICHAEL,
MASCARENO EDUARDO,
SIDDIQUI M.A.Q.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb09219.x
Subject(s) - signal transduction , muscle hypertrophy , microbiology and biotechnology , angiotensin ii , biology , intracellular , myocyte , endocrinology , medicine , cell , downregulation and upregulation , gene , biochemistry , blood pressure
A bstract : Cardiac hypertrophy results from the enlargement of cardiac muscle and fibroblast cells. This abnormal pattern of growth can be elicited by a number of hypertrophic agents, such as cytokines and hormones that participate in normal cell‐cell signaling events during development. Under conditions yet to be defined, these same signaling molecules can cause hypertrophy of the heart. Intracellular signal transduction pathways appear to be the prime means by which the hypertrophic signal is transduced in cardiomyocytes. There is no evidence that the signal transduction pathways in hypertrophic cardiomyocytes differ from those of normal cardiomyocytes. Perhaps the signal itself is aberrant, mistimed, misplaced, or occurring at non‐physiological concentrations. Alternatively, as a quiescent cell, the cardiomyocyte may not be able to respond completely to a growth signal by turning on its proliferative machinery. Three avenues of research are described: (1) the study of the upregulation of the cardiac MLC‐2 gene, (2) STAT proteins and activation of angiotensin II, and (3) hypertrophy as a perturbation of cell cycle controls.