ライフサイエンスコーパス: muscle degeneration

1 synaptic transmission that precedes nerve or muscle degeneration.

2 3 is expressed in satellite cells only after muscle degeneration.

3 and show that the absence of desmin leads to muscle degeneration.

4 vents occurring during the entire process of muscle degeneration.

5 taneous activities and histological signs of muscle degeneration.

6 GNE myopathy mice that have ongoing, active muscle degeneration.

7 ransgenic mouse model that develops profound muscle degeneration.

8 lateralis muscles and highly correlate with muscle degeneration.

9 transport S1P) can also suppress dystrophic muscle degeneration.

10 al role in mediating cancer-related skeletal muscle degeneration.

11 of the molecular pathomechanisms underlying muscle degeneration.

12 d that alterations in its activity result in muscle degeneration.

13 nd find that these manipulations also reduce muscle degeneration.

14 n conjunction with integrin alpha6 to reduce muscle degeneration.

15 uated tolerance to stress that could trigger muscle degeneration.

16 e, which leads to structural instability and muscle degeneration.

17 a perturbation of laminin expression before muscle degeneration.

18 utation leads to progressive lethal skeletal muscle degeneration.

19 a progressive and fatal genetic disorder of muscle degeneration.

20 -/- double mutants exhibit an early onset of muscle degeneration.

21 nt levels accelerated apoptosis and skeletal muscle degeneration.

22 nts in IBM pathology and subsequent skeletal muscle degeneration.

23 ciated with muscle injury or disease-related muscle degeneration.

24 in chronic inflammation and severe skeletal muscle degeneration.

25 s exhibit mitochondrial pathology and flight muscle degeneration.

26 unique model for understanding mechanisms of muscle degeneration.

27 s in coordinated movement and can also cause muscle degeneration.

28 iseases and are characterized by progressive muscle degeneration.

29 hin and that AQP4 is lost after the onset of muscle degeneration.

30 her therapies deal with secondary aspects of muscle degeneration, aiming, for example, at reducing in

31 l pathology is the earliest manifestation of muscle degeneration and a prominent characteristic of in

32 nteractions, giving rise to both progressive muscle degeneration and abnormal neuronal migration in t

33 Muscle degeneration and apoptosis of myonuclei in all fi

34 CTX)-mediated transient acute mouse model of muscle degeneration and compared the cardinal features w

35 muscle along with a significant decrease in muscle degeneration and concentrations of serum creatine

36 henotypes: decreased mobility, age-dependent muscle degeneration and defective photoreceptor path-fin

37 These data demonstrate that, in addition to muscle degeneration and dystrophy, impaired neuromuscula

38 n deficiency causes muscle membrane lesions, muscle degeneration and eventually death in afflicted in

39 , triggered by NF-kappaB activation, promote muscle degeneration and failure of muscle regeneration.

40 The Serpina3n transgene mitigated muscle degeneration and fibrosis, reduced creatine kinas

41 -) background substantially reduced skeletal muscle degeneration and histopathology compared with the

42 RH2 mutation as a novel driver of congenital muscle degeneration and identifies a potential novel tar

43 Conversely, the flight muscle degeneration and mitochondrial morphological alte

44 ranscriptional alterations that occur during muscle degeneration and performed a genetic screen for p

45 VI-truncated laminin alpha2-chain results in muscle degeneration and peripheral nerve dysmyelination

46 muscular dystrophy (DMD) is characterized by muscle degeneration and progressive weakness.

47 ase characterized by early onset of skeletal muscle degeneration and progressive weakness.

48 eased slow fiber (type 1) density, increased muscle degeneration and regeneration in aged muscles, de

49 elop a progressive myopathy characterized by muscle degeneration and regeneration, and abnormal metab

50 an also be a common secondary consequence of muscle degeneration and regeneration.

51 dystrophic mdx mouse, a model for continuous muscle degeneration and regeneration.

52 Loss of gamma-sarcoglycan (gamma-SG) induces muscle degeneration and signaling defects in response to

53 n-induced muscle injury are not required for muscle degeneration and the dystrophic process.

54 es are characterized by distinct patterns of muscle degeneration and this helps in selecting other re

55 angiogenesis and limb salvage while reducing muscle degeneration and tissue fibrosis.

56 In these diseases, progressive skeletal muscle degeneration and weakness contribute to cardiac d

57 ide accumulation, mitochondrial dysfunction, muscle degeneration, and cardiac malfunction, which were

58 he relationship between IBM autoimmunity and muscle degeneration, and develop an IBM blood test with

59 lies are flightless, showing indirect flight muscle degeneration, and females are sterile, showing di

60 inery is responsible for dysferlin-deficient muscle degeneration, and highlight the importance of thi

61 ction resulting in male sterility, apoptotic muscle degeneration, and minor loss of dopamine neurons

62 epidermis, abnormal hair follicles, cardiac muscle degeneration, and reduced amount of collagen and

63 oss of luciferase expression associated with muscle degeneration, and that protection was enhanced by

64 The mechanisms involved in muscle degeneration are not clearly defined, but recent

65 The associated fatigue and muscle degeneration are proposed to result from prolonge

66 phenotypes (fin erosion, cell apoptosis and muscle degeneration) are direct symptoms of infection.

67 -) mice exhibit differences in the extent of muscle degeneration between muscle groups with muscles e

68 Alendronate treatment did not ameliorate muscle degeneration, but demonstrated a limited enhancem

69 scle pathology with significant reduction in muscle degeneration, but had no effect on serum creatine

70 en show cognitive impairment, in addition to muscle degeneration caused by dystrophin gene defects.

71 xpression of drp1, rescues the phenotypes of muscle degeneration, cell death, and mitochondrial abnor

72 Muscle degeneration, denervation, neuromuscular [neuromu

73 Na+ overload may cause muscle degeneration developing with age.

74 NL3 activity in myogenic cells could lead to muscle degeneration disorders such as myotonic dystrophy

75 genetic disease characterized by progressive muscle degeneration due to mutations in the dystrophin g

76 e loss of spinal cord motor neurons, reduces muscle degeneration, improves muscle fiber thickness and

77 However, the mechanisms leading to muscle degeneration in DMD are poorly understood.

78 is associated with swollen mitochondria and muscle degeneration in Drosophila melanogaster, as well

79 on substantially affect skeletal and cardiac muscle degeneration in Duchenne muscular dystrophy.

80 nctional, and metabolic changes conducive to muscle degeneration in Krabbe disease using the murine (

81 the importance of oxidative stress-mediated muscle degeneration in muscular dystrophy, and reveal th

82 o accelerate muscle regeneration and to slow muscle degeneration in myositis, focusing primarily on i

83 Finally, the mechanism of cardiac and muscle degeneration in myotonic dystrophy has been re-ev

84 in this novel cell adhesion pathway, reduces muscle degeneration in zebrafish with intact integrin re

85 ions in the dystrophin gene, involves severe muscle degeneration, inflammation, fibrosis, and early d

86 ouble-knockout strains displayed exacerbated muscle degeneration, inflammation, fibrosis, and reduced

87 Skeletal muscle degeneration is a complication arising from a var

88 dult myoblasts called satellite cells during muscle degeneration is an important aspect of muscle reg

89 We demonstrate that muscle degeneration is dependent on exercise and force p

90 DMD, we show here that dystrophin-dependent muscle degeneration is likely to be cell autonomous and

91 model of muscular dystrophy (mdx), in which muscle degeneration is rapidly followed by regeneration.

92 hi myopathy, but the mechanism that leads to muscle degeneration is unknown.

93 ly SMT C1100 treatment significantly reduced muscle degeneration leading to improved muscle function.

94 m in vivo and in vitro studies suggests that muscle degeneration may be secondary to an increased sus

95 alysis indicates that, prior to the onset of muscle degeneration, mutant muscles are hyperinnervated.

96 This initiates a chain reaction of muscle degeneration, necrosis, inflammation and fibrosis

97 hogenesis suggests that at least part of the muscle degeneration observed in DMD patients may result

98 ibit different roles in dystrophin-dependent muscle degeneration occurring in a C. elegans model of D

99 athogenic process, but how it contributes to muscle degeneration of ALS is not known.

100 es can take many forms, from the progressive muscle degeneration of dystrophies to the childhood canc

101 previous study showed that in the context of muscle degeneration on a mdx (dystrophin null) genetic b

102 maintain minimal muscle force but not arrest muscle degeneration or necrosis.

103 mplex and significantly reduced the level of muscle degeneration over uninjected controls.

104 risingly, we have found that the progressive muscle degeneration phenotype of sapje mutant zebrafish

105 emma integrity, observed at the onset of the muscle degeneration process, triggers subcellular conseq

106 ered position and size, vacuoli and signs of muscle degeneration-regeneration were observed in head,

107 Muscle degeneration/regeneration experiments revealed th

108 ells activate and proliferate in response to muscle degeneration, resulting in an increase in the lev

109 s, with the markedly depleted dystrophin and muscle degeneration seen in early DMD.

110 Finally, in old mdx mice with severe muscle degeneration, simvastatin enhanced diaphragm forc

111 omozygous mutants of tardbp and tardbpl show muscle degeneration, strongly reduced blood circulation,

112 Usage-dependent muscle degeneration suggests a role for BAG3 in supporti

113 trophy (DMD) is characterized by progressive muscle degeneration that results from the absence of dys

114 lycoprotein complex assembly, but to prevent muscle degeneration the expression of a functional dystr

115 in histopathology but ultimately exacerbates muscle degeneration; this effect was not observed in dys

116 e, the role of NF-kappaB in cytokine-induced muscle degeneration was explored.

117 ential of targeting myostatin in settings of muscle degeneration, we crossed myostatin null mutant mi

118 Our analysis of drpr mutant flies revealed muscle degeneration with fiber size variability and vacu