Uremic Cardiomyopathy and Insulin Resistance
Author(s) -
David Semple,
Katie Smith,
Sunil Bhandari,
AnneMarie L. Seymour
Publication year - 2010
Publication title -
journal of the american society of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.451
H-Index - 279
eISSN - 1533-3450
pISSN - 1046-6673
DOI - 10.1681/asn.2009090900
Subject(s) - insulin resistance , medicine , protein kinase b , heart failure , cardiomyopathy , insulin , endocrinology , angiogenesis , cardiology , signal transduction , biology , biochemistry
Uremic cardiomyopathy is a classic complication of chronic renal failure whose cause is unclear and treatment remains disappointing. Insulin resistance is an independent predictor of cardiovascular mortality in chronic renal failure. Underlying insulin resistance are defects in insulin signaling through the protein kinase, Akt. Akt acts as a nodal point in the control of both the metabolic and pleiotropic effects of insulin. Imbalance among these effects leads to cardiac hypertrophy, fibrosis, and apoptosis; less angiogenesis; metabolic remodeling; and altered calcium cycling, all key features of uremic cardiomyopathy. Here we consider the role of Akt in the development of uremic cardiomyopathy, drawing parallels from models of hypertrophic cardiac disease.
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