ライフサイエンスコーパス: cellular hypertrophy

1 s in vitro activated autophagy and inhibited cellular hypertrophy.

2 ls, which increase myocyte number and reduce cellular hypertrophy.

3 ding to cell cycle arrest and instigation of cellular hypertrophy.

4 1), which activates Rap-family G proteins in cellular hypertrophy.

5 reduction of RPE-characteristic proteins and cellular hypertrophy.

6 to transcriptional signaling associated with cellular hypertrophy.

7 and MAP kinase pathways and is important for cellular hypertrophy.

8 ccurred without any histological evidence of cellular hypertrophy.

9 heart is a marker of fibrosis rather than of cellular hypertrophy.

10 l roles for class II HDACs in the control of cellular hypertrophy.

11 ctin expression, stress fiber formation, and cellular hypertrophy.

12 rference reduces both H3 phosphorylation and cellular hypertrophy.

13 diac cells and is accompanied by concomitant cellular hypertrophy.

14 Nutrient overabundance is known to promote cellular hypertrophy, a significant pathological event i

15 Focusing on the mandible, we observed that cellular hypertrophy and hyperplasia depended upon Ca2+

16 Exciting new drugs inhibiting fibrosis, cellular hypertrophy and improving cell-cell communicati

17 However, compensatory mechanisms, such as cellular hypertrophy and increased expression of the rat

18 Cellular hypertrophy and increased I(ss) amplitudes were

19 Epac1 transfection led to cellular hypertrophy and increased protein synthesis, wh

20 signal, premature differentiation results in cellular hypertrophy and newborn mice develop a dilated

21 rphogenesis of the mammary gland, and caused cellular hypertrophy and nuclear abnormalities.

22 ardiomyocyte in mouse left ventricles led to cellular hypertrophy and reduced expression of connexin4

23 n procedure became reactive, as evidenced by cellular hypertrophy and up-regulation of glial fibrilla

24 h glucose on cell growth (e.g., induction of cellular hypertrophy) and the stimulation of collagen bi

25 fibrillary acidic protein (GFAP) expression, cellular hypertrophy, and astrocyte proliferation.

26 ta (TGF-beta) mRNA and bioactivity, promotes cellular hypertrophy, and increases collagen synthesis i

27 ose stimulation of global protein synthesis, cellular hypertrophy, and matrix laminin and type IV col

28 tifocal interstitial inflammation, fibrosis, cellular hypertrophy, and occasional myocyte degeneratio

29 nduction is not an obligatory consequence of cellular hypertrophy, and that beta-MHC-expressing cells

30 sion, the enhanced cardiac myocyte death and cellular hypertrophy, are concomitant with ventricular d

31 -contraction coupling, and not regression of cellular hypertrophy, are specifically associated with c

32 ccurred because of a generalized response to cellular hypertrophy, betaARK activity was measured in t

33 ppears not to be related to the induction of cellular hypertrophy but to possibly be related to neuro

34 uppress astroglial DNA synthesis and promote cellular hypertrophy by inhibiting Ca(2+)-dependent Ca2+

35 or iCMs, as seen by enhanced polynucleation, cellular hypertrophy, gene expression, and metabolic rep

36 ological analysis confirmed profound myocyte cellular hypertrophy in AdvFGF-5 treated myocardium (19.

37 The hypothesis that cellular hypertrophy in congestive heart failure (CHF) m

38 The hypothesis that cellular hypertrophy in congestive heart failure (CHF) m

39 Red was more potent than CSQ2-WT in inducing cellular hypertrophy in cultured neonatal cardiomyocytes

40 lar smooth muscle cell protein synthesis and cellular hypertrophy in response to angiotensin II (Ang

41 ion of Agt and TGF-beta1 mRNA expression and cellular hypertrophy in RPTCs.

42 lts in morphological abnormalities including cellular hypertrophy in SY5Y cells and differentiated mo

43 Delivery of BMC populations promotes cellular hypertrophy in the border and infarcted regions

44 histologic organ of Corti changes including cellular hypertrophy in the region of the IHC and greate

45 boxane A2 receptor (TPr) stimulation induces cellular hypertrophy in vascular smooth muscle cells (VS

46 A case in point is cellular hypertrophy in which increased amounts of genet

47 rgan-size control that involves compensatory cellular hypertrophy induced by physical parameters.

48 These studies suggest that the regression of cellular hypertrophy is a major contributor to the "reve

49 This "compensatory cellular hypertrophy" is implemented by acceleration of

50 The cytoplasm-predominant protein caused cellular hypertrophy limited to the soma and led to incr

51 Methods to phenotype cellular hypertrophy noninvasively are limited.

52 Cellular hypertrophy, or growth without division, is an

53 ese AP waveform changes were associated with cellular hypertrophy, reduced current densities for L- a

54 essing cells displayed significantly greater cellular hypertrophy relative to mock-transfected cells.

55 Cellular hypertrophy requires coordinated regulation of

56 ) current amplitudes paralleled the observed cellular hypertrophy, resulting in normalized or increas

57 of MEK1/2, ERK1/2, and p90RSK and prevented cellular hypertrophy, sarcomere reorganization, and prot

58 ceptor, resulted in upregulation of GFAP and cellular hypertrophy specifically in astrocyte populatio

59 cyte proliferation and regression of myocyte cellular hypertrophy support a common mechanism of cardi

60 ult ventricular myocytes in vitro results in cellular hypertrophy, the changes in myocyte volume and

61 oss of local tissue volume triggers sporadic cellular hypertrophy to repair the tissue.

62 The mechanism of the cellular hypertrophy was due to uncoupling of hypertroph

63 actor, used as a molecular marker of myocyte cellular hypertrophy, was greater at 3 days in 4-month-o

64 n activation, [3H]leucine incorporation, and cellular hypertrophy were inhibited by pretreatment with

65 Expression of p21CIP in VSMCs leads to cellular hypertrophy, whereas expression of p21CIP in en

66 mooth muscle cell cycle traversal can induce cellular hypertrophy, which parallels changes observed i

67 Both 12(S)-HETE and AngII increased cellular hypertrophy with similar potency, and this was