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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 mic stress on the mammalian heart results in compensatory hypertrophy and activation of the unfolded
13  filtration rate (GFR) after they experience compensatory hypertrophy and hyperfiltration in their re
14 yocardial dysfunction that occurs early with compensatory hypertrophy, and improves following relief
15  we observed that TAK1 is upregulated during compensatory hypertrophy but downregulated in end-stage
16 verload plays an essential role in mediating compensatory hypertrophy by inducing the release of Bcl-
17                           Although initially compensatory, hypertrophy can proceed by unknown mechani
18 fy signaling processes associated with renal compensatory hypertrophy, demonstrating that the lipid-a
19 depressed myocardial contraction leads to a 'compensatory' hypertrophy has proven inconsistent with l
20 ue and myocytes were maintained during early compensatory hypertrophy in 6-week aortic stenosis anima
21 the role of CLP-1 in the mechanism governing compensatory hypertrophy in cardiomyocytes.
22 t persistent inhibition of GSK-3beta induces compensatory hypertrophy, inhibits apoptosis and fibrosi
23                                          The compensatory hypertrophy normally found in mdx muscles w
24  half of the normal number of nephrons, with compensatory hypertrophy of the glomeruli.
25 tion-induced shrinkage of the right lobe and compensatory hypertrophy of the left lobe is difficult f
26 e regenerative response after PVE leading to compensatory hypertrophy of the nonembolized liver segme
27  USG and MRI showed left renal agenesis with compensatory hypertrophy of the right kidney, uterus did
28 ng atrophy of RPSA-deficient cardiomyocytes, compensatory hypertrophy of unaffected cardiomyocytes, l
29                                         With compensatory hypertrophy, peak wall stress normalized by
30                                        Renal compensatory hypertrophy (RCH) restores normal kidney fu
31  shown to be crucial for the transition from compensatory hypertrophy to cardiac failure.
32 bB receptor signaling in the transition from compensatory hypertrophy to failure.