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Author Adiga, Indira ♦ Nair, R. R.
Source Sree Chitra Tirunal Institute for Medical Sciences & Technology
Content type Text
Publisher Cell Biochemistry and Function
File Format PDF
Language English
Subject Domain (in DDC) Technology ♦ Medicine & health ♦ Diseases
Subject Domain (in MeSH) Cardiovascular Diseases ♦ Diseases ♦ Cell Physiological Phenomena ♦ Biological Sciences
Subject Keyword Cardiology
Abstract The heart responds to an increased demand arising due to physiological stimuli or pathological insults by hypertrophy of myocytes. Reactive oxygen species (ROS) have recently been identified as the molecular intermediates in the translation of mechanical stimuli to cellular response. Different signal transduction pathways have been implicated with cardiac hypertrophy, prominent among them being, mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and calcineurin. It remains unclear whether the ROS induced hypertrophy is mediated through one or more of these pathways. This study was taken up with the objective to affirm the role of ROS in the induction of cardiomyocyte hypertrophy and examine the contribution of specific pathways in the mediation of the hypertrophic response. The cellular response to enzyme-generated reactive oxygen species was examined in cultured cells from newborn rat heart. Pathway specific inhibitors were used to identify the role of each pathway in the mediation of cellular hypertrophy. Cellular hypertrophy in response to hypoxanthine-xanthine oxidase was prevented by inhibition of any one of the pathways; leading to the inference that oxidative stress induced hypertrophy is mediated by coordinative regulation of the three major pathways. Copyright (c) 2008 John Wiley & Sons, Ltd.
Education Level UG and PG
Learning Resource Type Article
Educational Framework Medical Council of India (MCI)
Journal CELL BIOCHEMISTRY AND FUNCTION
Volume Number 26
Issue Number 3
Page Count 6
Starting Page 346
Ending Page 351