TY - JOUR
T1 - Autophagy in cardiac plasticity and disease
AU - Hill, Joseph A
N1 - Funding Information:
We are grateful to members of the Hill laboratory for valuable suggestions and comments. This work was supported by grants from the National Institutes of Health NIH (Grants No. HL-075173, HL-080144, and HL-090842), The American Heart Association (AHA; Grant No. 0640084N), and the AHA—Jon Holden DeHaan Foundation.
PY - 2011/3
Y1 - 2011/3
N2 - The heart is a highly plastic organ. In response to the physiological stress of normal life, as well as the pathological stress of disease, the myocardium manifests robust and rapid changes in mass. In the context of disease-associated stress, this myocardial remodeling response can culminate in ventricular thinning, mechanical dysfunction, and a clinical syndrome of heart failure. Recently, autophagy, a process of cellular cannibalization, has been implicated in many of these remodeling reactions. In some settings, the autophagic response is beneficial and pro-survival; in other contexts, it is maladaptive and promotes disease progression. Together, these observations raise the intriguing prospect of targeting maladaptive autophagy and advancing cell survival-promoting, adaptive autophagy to benefit patients with heart disease.
AB - The heart is a highly plastic organ. In response to the physiological stress of normal life, as well as the pathological stress of disease, the myocardium manifests robust and rapid changes in mass. In the context of disease-associated stress, this myocardial remodeling response can culminate in ventricular thinning, mechanical dysfunction, and a clinical syndrome of heart failure. Recently, autophagy, a process of cellular cannibalization, has been implicated in many of these remodeling reactions. In some settings, the autophagic response is beneficial and pro-survival; in other contexts, it is maladaptive and promotes disease progression. Together, these observations raise the intriguing prospect of targeting maladaptive autophagy and advancing cell survival-promoting, adaptive autophagy to benefit patients with heart disease.
KW - Autophagy
KW - Heart failure
KW - Hypertrophy
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U2 - 10.1007/s00246-010-9883-6
DO - 10.1007/s00246-010-9883-6
M3 - Article
C2 - 21249349
AN - SCOPUS:79953762724
SN - 0172-0643
VL - 32
SP - 282
EP - 289
JO - Pediatric Cardiology
JF - Pediatric Cardiology
IS - 3
ER -