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1 yperactivity, hypertrophic gene response and cellular hypertrophy.
2 rference reduces both H3 phosphorylation and cellular hypertrophy.
3 diac cells and is accompanied by concomitant cellular hypertrophy.
4 ls, which increase myocyte number and reduce cellular hypertrophy.
5 ding to cell cycle arrest and instigation of cellular hypertrophy.
6 1), which activates Rap-family G proteins in cellular hypertrophy.
7 reduction of RPE-characteristic proteins and cellular hypertrophy.
8 to transcriptional signaling associated with cellular hypertrophy.
9 and MAP kinase pathways and is important for cellular hypertrophy.
10 ccurred without any histological evidence of cellular hypertrophy.
11 f glial fibrillary acidic protein (GFAP) and cellular hypertrophy.
12 heart is a marker of fibrosis rather than of cellular hypertrophy.
13 l roles for class II HDACs in the control of cellular hypertrophy.
14 s in vitro activated autophagy and inhibited cellular hypertrophy.
15 ctin expression, stress fiber formation, and cellular hypertrophy.
16 ntractile force, and contractility-dependent cellular hypertrophy.
17  glycolysis that preceded the development of cellular hypertrophy.
18       Palmitate treatment was used to induce cellular hypertrophy.
19 g which cardiomyocyte number doubled without cellular hypertrophy.
20   Nutrient overabundance is known to promote cellular hypertrophy, a significant pathological event i
21    RV myocytes from HF rats show significant cellular hypertrophy accompanied with a disruption of tr
22 ed by increased left ventricular mass due to cellular hypertrophy and extracellular matrix expansion.
23   Focusing on the mandible, we observed that cellular hypertrophy and hyperplasia depended upon Ca2+
24 t only reduces contractility but also causes cellular hypertrophy and impairs cardiomyocytes' ability
25      Exciting new drugs inhibiting fibrosis, cellular hypertrophy and improving cell-cell communicati
26    However, compensatory mechanisms, such as cellular hypertrophy and increased expression of the rat
27                                              Cellular hypertrophy and increased I(ss) amplitudes were
28                    Epac1 transfection led to cellular hypertrophy and increased protein synthesis, wh
29 em cell-derived cardiomyocytes recapitulated cellular hypertrophy and increased resting calcium, whic
30 signal, premature differentiation results in cellular hypertrophy and newborn mice develop a dilated
31 rphogenesis of the mammary gland, and caused cellular hypertrophy and nuclear abnormalities.
32 ardiomyocyte in mouse left ventricles led to cellular hypertrophy and reduced expression of connexin4
33  Changes in metabolism induce early adaptive cellular hypertrophy and reorganization of the actin cyt
34 ility, increased metabolic requirements, and cellular hypertrophy and the etiological fraction (0.93
35 n procedure became reactive, as evidenced by cellular hypertrophy and up-regulation of glial fibrilla
36 h glucose on cell growth (e.g., induction of cellular hypertrophy) and the stimulation of collagen bi
37 fibrillary acidic protein (GFAP) expression, cellular hypertrophy, and astrocyte proliferation.
38 ta (TGF-beta) mRNA and bioactivity, promotes cellular hypertrophy, and increases collagen synthesis i
39 ose stimulation of global protein synthesis, cellular hypertrophy, and matrix laminin and type IV col
40 tifocal interstitial inflammation, fibrosis, cellular hypertrophy, and occasional myocyte degeneratio
41 nduction is not an obligatory consequence of cellular hypertrophy, and that beta-MHC-expressing cells
42 expansion (diffuse interstitial fibrosis) or cellular hypertrophy, and whether residual RV remodeling
43 sion, the enhanced cardiac myocyte death and cellular hypertrophy, are concomitant with ventricular d
44 -contraction coupling, and not regression of cellular hypertrophy, are specifically associated with c
45 ccurred because of a generalized response to cellular hypertrophy, betaARK activity was measured in t
46 ppears not to be related to the induction of cellular hypertrophy but to possibly be related to neuro
47 uppress astroglial DNA synthesis and promote cellular hypertrophy by inhibiting Ca(2+)-dependent Ca2+
48 ptosis but which differs by causing enormous cellular hypertrophy followed by cleavage of the cell in
49 or iCMs, as seen by enhanced polynucleation, cellular hypertrophy, gene expression, and metabolic rep
50 ological analysis confirmed profound myocyte cellular hypertrophy in AdvFGF-5 treated myocardium (19.
51                          The hypothesis that cellular hypertrophy in congestive heart failure (CHF) m
52                          The hypothesis that cellular hypertrophy in congestive heart failure (CHF) m
53 Red was more potent than CSQ2-WT in inducing cellular hypertrophy in cultured neonatal cardiomyocytes
54 lar smooth muscle cell protein synthesis and cellular hypertrophy in response to angiotensin II (Ang
55 ion of Agt and TGF-beta1 mRNA expression and cellular hypertrophy in RPTCs.
56 lts in morphological abnormalities including cellular hypertrophy in SY5Y cells and differentiated mo
57         Delivery of BMC populations promotes cellular hypertrophy in the border and infarcted regions
58  histologic organ of Corti changes including cellular hypertrophy in the region of the IHC and greate
59 boxane A2 receptor (TPr) stimulation induces cellular hypertrophy in vascular smooth muscle cells (VS
60                           A case in point is cellular hypertrophy in which increased amounts of genet
61 rgan-size control that involves compensatory cellular hypertrophy induced by physical parameters.
62 These studies suggest that the regression of cellular hypertrophy is a major contributor to the "reve
63                           This "compensatory cellular hypertrophy" is implemented by acceleration of
64     The cytoplasm-predominant protein caused cellular hypertrophy limited to the soma and led to incr
65 n cerebellar Purkinje cells (PCs) results in cellular hypertrophy, neurodegeneration, and autism-like
66                         Methods to phenotype cellular hypertrophy noninvasively are limited.
67     Adipose tissue can expand either through cellular hypertrophy or hyperplasia, with the former cor
68                                              Cellular hypertrophy, or growth without division, is an
69 ese AP waveform changes were associated with cellular hypertrophy, reduced current densities for L- a
70                                     Although cellular hypertrophy regresses and diastolic stiffness n
71 essing cells displayed significantly greater cellular hypertrophy relative to mock-transfected cells.
72                                              Cellular hypertrophy requires coordinated regulation of
73 ) current amplitudes paralleled the observed cellular hypertrophy, resulting in normalized or increas
74  of MEK1/2, ERK1/2, and p90RSK and prevented cellular hypertrophy, sarcomere reorganization, and prot
75 ceptor, resulted in upregulation of GFAP and cellular hypertrophy specifically in astrocyte populatio
76 cyte proliferation and regression of myocyte cellular hypertrophy support a common mechanism of cardi
77 ult ventricular myocytes in vitro results in cellular hypertrophy, the changes in myocyte volume and
78 oss of local tissue volume triggers sporadic cellular hypertrophy to repair the tissue.
79 ithelium and endothelium exhibit DNA damage, cellular hypertrophy, upregulation of inflammatory cytok
80 erties using video-based edge detection, and cellular hypertrophy using immunohistochemistry.
81                         The mechanism of the cellular hypertrophy was due to uncoupling of hypertroph
82                                              Cellular hypertrophy was prevented in the P710R cells by
83 actor, used as a molecular marker of myocyte cellular hypertrophy, was greater at 3 days in 4-month-o
84 n activation, [3H]leucine incorporation, and cellular hypertrophy were inhibited by pretreatment with
85       Expression of p21CIP in VSMCs leads to cellular hypertrophy, whereas expression of p21CIP in en
86 mooth muscle cell cycle traversal can induce cellular hypertrophy, which parallels changes observed i
87          Both 12(S)-HETE and AngII increased cellular hypertrophy with similar potency, and this was
88 hanges in nuclear parameters, in addition to cellular hypertrophy, with SNRK knockdown.