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1 ts roles in promoting beta cell survival and compensatory hypertrophy.
2 (RLC) in cardiac muscle is proposed to cause compensatory hypertrophy.
3 formance is preserved despite attenuation of compensatory hypertrophy.
4 optosis versus the control mice that exhibit compensatory hypertrophy.
5 an important role in renal tubulogenesis and compensatory hypertrophy.
6 cyte contractility, providing an impetus for compensatory hypertrophy.
7 ibrosis, with the remaining cells undergoing compensatory hypertrophy.
8 tion to pressure overload and development of compensatory hypertrophy.
9 ncorporate into sarcomeres, which may elicit compensatory hypertrophy.
10 e with ascending aortic stenosis (AS) during compensatory hypertrophy (4-week AS) and the later stage
11 ifying the molecular mechanisms activated in compensatory hypertrophy and absent during decompensatio
12 filtration rate (GFR) after they experience compensatory hypertrophy and hyperfiltration in their re
13 yocardial dysfunction that occurs early with compensatory hypertrophy, and improves following relief
14 we observed that TAK1 is upregulated during compensatory hypertrophy but downregulated in end-stage
16 depressed myocardial contraction leads to a 'compensatory' hypertrophy has proven inconsistent with l
17 ue and myocytes were maintained during early compensatory hypertrophy in 6-week aortic stenosis anima
19 t persistent inhibition of GSK-3beta induces compensatory hypertrophy, inhibits apoptosis and fibrosi
22 e regenerative response after PVE leading to compensatory hypertrophy of the nonembolized liver segme
23 USG and MRI showed left renal agenesis with compensatory hypertrophy of the right kidney, uterus did
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