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Molecular mechanisms of cardiac hypertrophy induced by toxicants

Content Provider	Springer Nature Link
Author	Chen, Qin M. Tu, Victoria C. Purdom, Sally Wood, June Dilley, Tarrah
Copyright Year	2001
Abstract	Cardiac hypertrophy is an end point of chronic cardiac toxicity from a number of toxicants. Doxorubicin, cocaine, acetaldehyde, monocrotaline, and azide are examples of these toxicants, which may induce hypertrophy by increasing oxidants, circulating levels of catecholamines, and hemodynamic load or by inducing hypoxia. We summarize here the major signal transduction pathways and common changes in gene expression found with the classical hypertrophy inducers angiotensin II, endothelin 1, and catecholamines. Activation of G-proteins, calcium signaling, phosphoinositide 3-kinase (PI3K), certain family members of protein kinase Cs (PKCs), and three branches of mitogen-activated protein kinases (MAPKs), i.e. extracellular signal-regulated kinases (ERKs), p38, and c-Jun N-terminal kinases (JNKs), are important for developing a hypertrophic phenotype in cardiomyocytes. Characteristic changes of gene expression in hypertrophy include the elevated transcription of atrial natriuretic factor (ANF), β-myosin heavy chain (βMHC), skeletal α-actin (SkA), certain variants of integrins and perhaps tubulin genes, and reduced expression of the sarcoplasmic reticulum proteins phospholamban and sarco(endo)plasmic reticulum Ca$^{2+}$-ATPase 2α (SERCA2α), and of the ryanodine receptors. Although which toxicants induce these molecular changes remains to be tested, increasing lines of evidence support that oxidants play a central role in cardiac hypertrophy. Oxidants activate small G-proteins, calcium signaling, P13K, PKCs, and MAPKs. Oxidants cause cardiomyocytes to enlarge in vitro. Recent developments in transgenic, genomic, and proteomic technologies will provide needed tools to reveal the mechanism of chronic cardiac toxicity at the cellular and molecular levels.
Starting Page	267
Ending Page	283
Page Count	17
File Format	PDF
ISSN	15307905
Journal	Cardiovascular Toxicology
Volume Number	1
Issue Number	4
e-ISSN	15590259
Language	English
Publisher	Humana Press
Publisher Date	2001-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Calcium kinases geneexpression atrial natriuretic factor oxidative stress hemodynamic overload catecholamines angiotensin II doxorubicin monocrotaline Pharmacology/Toxicology Cardiology
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Toxicology Cardiology and Cardiovascular Medicine

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