TY - JOUR
T1 - Autophagy in hypertensive heart disease
AU - Wang, Zhao
AU - Rothermel, Beverly A
AU - Hill, Joseph A
PY - 2010/3/19
Y1 - 2010/3/19
N2 - In response to hypertension, the heart manifests robust hypertrophic growth, which offsets load-induced elevations in wall stress. If sustained, this hypertrophic response is a major risk factor for systolic dysfunction and heart failure. Extensive research efforts have focused on the progression from hypertrophy to failure; however, precise understanding of underlying mechanisms remains elusive. Recently, autophagy, a process of cellular cannibalization, has been implicated. Autophagy is activated during ventricular hypertrophy, serving to maintain cellular homeostasis. Excessive autophagy eliminates, however, essential cellular elements and possibly provokes cell death, which together contribute to hypertension-related heart disease.
AB - In response to hypertension, the heart manifests robust hypertrophic growth, which offsets load-induced elevations in wall stress. If sustained, this hypertrophic response is a major risk factor for systolic dysfunction and heart failure. Extensive research efforts have focused on the progression from hypertrophy to failure; however, precise understanding of underlying mechanisms remains elusive. Recently, autophagy, a process of cellular cannibalization, has been implicated. Autophagy is activated during ventricular hypertrophy, serving to maintain cellular homeostasis. Excessive autophagy eliminates, however, essential cellular elements and possibly provokes cell death, which together contribute to hypertension-related heart disease.
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U2 - 10.1074/jbc.R109.025023
DO - 10.1074/jbc.R109.025023
M3 - Short survey
C2 - 20118246
AN - SCOPUS:77950576949
SN - 0021-9258
VL - 285
SP - 8509
EP - 8514
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 12
ER -