TY - JOUR
T1 - Metabolic stress in the myocardium
T2 - Adaptations of gene expression
AU - Crawford, Peter A.
AU - Schaffer, Jean E.
N1 - Funding Information:
This work was supported by grants from the NIH ( R01 DK064989 and P20 HL113444 to JES; R01 DK091538 to PAC) and from the Burroughs Wellcome Foundation ( 1005935 to JES).
PY - 2013/2
Y1 - 2013/2
N2 - The heart is one of the highest ATP consuming organs in mammalian organisms. Its metabolic function has evolved a remarkable degree of efficiency to meet high demand and plasticity in response to varying changes in energy substrate supply. Given the high flux of energy substrates and the centrality of their appropriate use for optimal cardiac function, it is not surprising that the heart has intricate signaling mechanisms through which it responds to metabolic stress. This review focuses on the changes in gene expression in myocardial and vascular tissues during metabolic stress that affect mRNAs and subsequent protein synthesis with an eye toward understanding the manner in which these changes effect adaptive and maladaptive responses of the heart. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".
AB - The heart is one of the highest ATP consuming organs in mammalian organisms. Its metabolic function has evolved a remarkable degree of efficiency to meet high demand and plasticity in response to varying changes in energy substrate supply. Given the high flux of energy substrates and the centrality of their appropriate use for optimal cardiac function, it is not surprising that the heart has intricate signaling mechanisms through which it responds to metabolic stress. This review focuses on the changes in gene expression in myocardial and vascular tissues during metabolic stress that affect mRNAs and subsequent protein synthesis with an eye toward understanding the manner in which these changes effect adaptive and maladaptive responses of the heart. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".
KW - Diabetic cardiomyopathy
KW - Histone deacetylation
KW - Ischemia-reperfusion
KW - MiRNA
KW - Nuclear receptor transcription factor
KW - Pathological hypertrophy
KW - Protein translation
UR - http://www.scopus.com/inward/record.url?scp=84872683146&partnerID=8YFLogxK
U2 - 10.1016/j.yjmcc.2012.06.008
DO - 10.1016/j.yjmcc.2012.06.008
M3 - Review article
C2 - 22728216
AN - SCOPUS:84872683146
SN - 0022-2828
VL - 55
SP - 130
EP - 138
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
IS - 1
ER -