ライフサイエンスコーパス: muscle hypertrophy

1 ntially expressed mRNA during early skeletal muscle hypertrophy.

2 nterior (TA) muscle has been shown to elicit muscle hypertrophy.

3 hypothesize that it plays a role in skeletal muscle hypertrophy.

4 additional signals are required for skeletal muscle hypertrophy.

5 muscle fibers, but no evidence for skeletal muscle hypertrophy.

6 s, and fibrosis, as well as oviductal smooth muscle hypertrophy.

7 ctivating mutations of myostatin have marked muscle hypertrophy.

8 stem cell fusion during physiological adult muscle hypertrophy.

9 PGC1alpha mRNA and has been shown to promote muscle hypertrophy.

10 mass, while deletion of Tp53inp2 resulted in muscle hypertrophy.

11 t is unrelated to mucus metaplasia or smooth muscle hypertrophy.

12 in vitro and in vivo induces robust skeletal muscle hypertrophy.

13 fically in myofibers is sufficient to induce muscle hypertrophy.

14 and coordinates factors involved in skeletal muscle hypertrophy.

15 Cripto accelerates regeneration, leading to muscle hypertrophy.

16 at ActRIIB inhibition results in significant muscle hypertrophy.

17 during mechanical overload-induced skeletal muscle hypertrophy.

18 chanism and is sufficient to induce skeletal muscle hypertrophy.

19 rmal kidney function exhibited mild skeletal muscle hypertrophy.

20 and sufficient for the induction of skeletal muscle hypertrophy.

21 n, whether mainly inflammation, fibrosis, or muscle hypertrophy.

22 ixed findings of inflammation, fibrosis, and muscle hypertrophy.

23 fibroblasts to stimulate myoblast fusion and muscle hypertrophy.

24 prolong mTORC1 signalling and contribute to muscle hypertrophy.

25 equired for GSK-3beta-mediated airway smooth muscle hypertrophy.

26 ons and measure wasting and exercise-induced muscle hypertrophy.

27 ht to be a critical step in the induction of muscle hypertrophy.

28 s that contribute to hypertension and smooth muscle hypertrophy.

29 ce the pathways normally leading to skeletal muscle hypertrophy.

30 ber-type switching, and cardiac and skeletal muscle hypertrophy.

31 king ribosome biogenesis central to skeletal muscle hypertrophy.

32 ack of glycolytic fibers as well as signs of muscle hypertrophy.

33 g in coordinating angiogenesis with skeletal muscle hypertrophy.

34 c subtype (inflammation, 5; fibrosis, 4; and muscle hypertrophy, 3), acute and chronic inflammation,

35 beta (GSK-3beta) inhibition in airway smooth muscle hypertrophy, a structural change found in patient

36 Moreover, we show that muscle hypertrophy after pharmacological blockade of thi

37 indicate that work overload induced skeletal muscle hypertrophy alters autocrine/paracrine signaling,

38 characterized by the inability to walk, leg muscle hypertrophy and a secondary deficiency of laminin

39 st that increased mechanical load can induce muscle hypertrophy and activate the Akt and p70(s6k) ind

40 GPR56 expression attenuates overload-induced muscle hypertrophy and associated anabolic signaling.

41 d unexpectedly myostatin, known mediators of muscle hypertrophy and atrophy, respectively.

42 ing the complex molecular systems underlying muscle hypertrophy and atrophy.

43 delivered IGF-1 genes induce local skeletal muscle hypertrophy and attenuate age-related skeletal mu

44 amycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effect

45 t cell hyperplasia and metaplasia and smooth muscle hypertrophy and fibrosis); levels of IgE, eotaxin

46 f (18)F-FDG PET/CT for differentiating fixed muscle hypertrophy and fibrotic stenoses from acute tran

47 top of GDF8 inhibition, leads to pronounced muscle hypertrophy and force production in mice and monk

48 r fasting or denervation without stimulating muscle hypertrophy and GHSR-1a-mediated activation of th

49 odulated PTEN/AKT signaling, which regulates muscle hypertrophy and growth, and induced apoptosis.

50 ed evidence of significant intestinal smooth muscle hypertrophy and hyperplasia associated with abnor

51 fibrosis, goblet cell metaplasia, and smooth muscle hypertrophy and hyperplasia).

52 Vector treatment also prevented pathological muscle hypertrophy and resulted in normal muscle weight

53 idence that endurance exercise can attenuate muscle hypertrophy and strength but the mechanistic unde

54 ting Akt will be useful in inducing skeletal muscle hypertrophy and that an increase in lean muscle m

55 ID1 and TSLP, inflammation, fibrosis, smooth muscle hypertrophy, and expression of inflammatory effec

56 arts exhibited atrial enlargement, papillary muscle hypertrophy, and fibrosis.

57 eness, atherosclerosis, angiogenesis, smooth muscle hypertrophy, and hyperplasia.

58 skeletal muscle atrophy, stimulated skeletal muscle hypertrophy, and increased strength and exercise

59 nd to enhance alpha7 integrin levels, induce muscle hypertrophy, and inhibit apoptosis in myotubes by

60 re all positively correlated with percentage muscle hypertrophy, and negatively correlated with the p

61 naling pathway through GPR56 which regulates muscle hypertrophy associated with resistance/loading-ty

62 ude bronchial wall thickening, airway smooth muscle hypertrophy, bronchiectasis and emphysema.

63 like growth factor 1 (IGF1) induces skeletal muscle hypertrophy by activating the IGF1R/IRS1/PI3K/Akt

64 t depending on the disease context, inducing muscle hypertrophy by myostatin blockade may have detrim

65 unctional overload model to induce plantaris muscle hypertrophy by surgically removing the soleus and

66 To evaluate whether promoting muscle hypertrophy can attenuate symptoms resulting from

67 hed model of pressure overload-induced heart muscle hypertrophy caused by transverse aortic constrict

68 Muscle hypertrophy coincided with significant elevations

69 Promoting skeletal muscle muscle hypertrophy could therefore have potential applic

70 and molecular mechanisms underlying skeletal muscle hypertrophy, expression profiles of translational

71 lthough the molecular mechanism for skeletal muscle hypertrophy has been well studied, it still is no

72 he significance of this process during adult muscle hypertrophy has not been explored.

73 and epithelium, diminished intestinal smooth muscle hypertrophy/hyperplasia, and impaired worm expuls

74 bservation that loss of myostatin results in muscle hypertrophy in a human subject.

75 erved, potent negative regulator of skeletal muscle hypertrophy in many species, from rodents to huma

76 hat myostatin/activin A inhibition can cause muscle hypertrophy in mice lacking either syndecan4 or P

77 to challenge in G allele carriers, promoting muscle hypertrophy in normal females, but increased dama

78 whole body protein metabolism or RT-induced muscle hypertrophy in older people.

79 e myogenesis in non-muscle cells, to promote muscle hypertrophy in postnatal mice, and to activate tr

80 Muscle hypertrophy in response to increasing demand is d

81 umption by older people may promote skeletal muscle hypertrophy in response to resistance training (R

82 owth factor (IGF) system in exercise-induced muscle hypertrophy in the context of RA.

83 inflammation, collagen deposition and smooth muscle hypertrophy in the lungs of a murine model of ova

84 control pathway contributes to airway smooth muscle hypertrophy in vitro and in vivo.

85 down of GPR56 attenuates PGC-1alpha4-induced muscle hypertrophy in vitro.

86 itro In mice, knockdown of AK017368 promoted muscle hypertrophy in vivo RNA molecules of AK017368 act

87 ent to induce rapid and significant skeletal muscle hypertrophy in vivo, accompanied by activation of

88 bronchial fibrosis, and peribronchial smooth muscle hypertrophy; increased levels of interleukin (IL)

89 ng the beta2-AR pathway can promote skeletal muscle hypertrophy independent of ligand administration,

90 s develop a spontaneous cardiac and skeletal muscle hypertrophy, indicating cooperative control of mu

91 and the role of satellite cells in mediating muscle hypertrophy induced by inhibition of this signali

92 A murine model of overload-induced muscle hypertrophy is associated with increased expressi

93 Airway smooth muscle hypertrophy is one of the hallmarks of airway rem

94 The mechanism linking the mutation to muscle hypertrophy is unclear but involves DLK1 overexpr

95 In skeletal muscle, hypertrophy is generally regarded as a beneficia

96 fibrosis (median, 50%; range, 40%-90%), and muscle hypertrophy (median, 20-fold thickening; range, 9

97 No patient with predominantly fibrosis or muscle hypertrophy (n = 7) had an SUL(max) greater than

98 elial cell proliferation and vascular smooth muscle hypertrophy of the small precapillary pulmonary a

99 ophy; and 3) identified secondary effects of muscle hypertrophy on body composition.

100 Mutations in MSTN gene can lead to muscle hypertrophy or double-muscled (DM) phenotype in c

101 ot show a significant difference in skeletal muscle hypertrophy or strength with resistance training.

102 ular myocilin plays a role as a regulator of muscle hypertrophy pathways, acting through the componen

103 to carry the mutation causing the callipyge muscle hypertrophy phenotype in sheep.

104 Coinciding with muscle hypertrophy, previously diminished muscle levels

105 s that provide the extra nuclei required for muscle hypertrophy, repair and maintenance.

106 mber of muscle groups trained influenced the muscle hypertrophy response to RT.

107 Skeletal muscle hypertrophy stimulated by clenbuterol, a beta2-ad

108 Papillary muscle hypertrophy that produced midcavitary obstruction

109 ks prior to denervation or tenotomy promoted muscle hypertrophy that was sufficient to preserve muscl

110 xtensive evidence implicating Ras in cardiac muscle hypertrophy, the mechanisms involved are unclear.

111 t satellite cells are necessary for skeletal muscle hypertrophy, the plantaris muscle of adult Pax7-D

112 Generalized muscle hypertrophy, transient weakness and depressed ten

113 For mdx mice of all ages, muscle hypertrophy was highly effective in the maintenan

114 Skeletal muscle hypertrophy was induced in the plantaris muscle u

115 Muscle hypertrophy was initiated by bilateral ablation o

116 the IGF-I receptor in load-induced skeletal muscle hypertrophy, we utilized a transgenic mouse model

117 taplasia, peribronchial fibrosis, and smooth muscle hypertrophy were quantitated on tissue sections.

118 d activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-AT

119 and may behave as a key modulator of smooth muscle hypertrophy, which is relevant for organ remodeli

120 ndividuals have a reduced capacity to induce muscle hypertrophy with resistance exercise (RE), which

121 udy, we; 1) characterized the development of muscle hypertrophy with respect to fiber type, age, and

122 was that strength training, which stimulates muscle hypertrophy, would help preserve both FFM and RMR