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1 s exhibit mitochondrial pathology and flight muscle degeneration.
2 unique model for understanding mechanisms of muscle degeneration.
3 s in coordinated movement and can also cause muscle degeneration.
4 iseases and are characterized by progressive muscle degeneration.
5 er conditions of cell stress and age-related muscle degeneration.
6 hin and that AQP4 is lost after the onset of muscle degeneration.
7 synaptic transmission that precedes nerve or muscle degeneration.
8 muscle or facilitate pathologic fibrosis and muscle degeneration.
9 3 is expressed in satellite cells only after muscle degeneration.
10 and show that the absence of desmin leads to muscle degeneration.
11 ing ABCD3 transcript in progressive skeletal muscle degeneration.
12 with potential clinical benefits in reducing muscle degeneration.
13 e use of cotreatments that decrease skeletal muscle degeneration.
14 al, with deficits in this process leading to muscle degeneration.
15 fficiently high editing efficiencies to halt muscle degeneration.
16 se proteins declines during aging leading to muscle degeneration.
17 keletal muscle homeostasis and prevent adult muscle degeneration.
18 d that alterations in its activity result in muscle degeneration.
19 uated tolerance to stress that could trigger muscle degeneration.
20 nt levels accelerated apoptosis and skeletal muscle degeneration.
21 vents occurring during the entire process of muscle degeneration.
22 ents disrupts costamere complexes to promote muscle degeneration.
23 taneous activities and histological signs of muscle degeneration.
24 GNE myopathy mice that have ongoing, active muscle degeneration.
25 ransgenic mouse model that develops profound muscle degeneration.
26 lateralis muscles and highly correlate with muscle degeneration.
27 -linked disease characterized by progressive muscle degeneration.
28 transport S1P) can also suppress dystrophic muscle degeneration.
29 al role in mediating cancer-related skeletal muscle degeneration.
30 of the molecular pathomechanisms underlying muscle degeneration.
31 nd find that these manipulations also reduce muscle degeneration.
32 ay be developed as a natural therapeutic for muscle degeneration.
33 n conjunction with integrin alpha6 to reduce muscle degeneration.
34 e, which leads to structural instability and muscle degeneration.
35 a perturbation of laminin expression before muscle degeneration.
36 utation leads to progressive lethal skeletal muscle degeneration.
37 MD) is characterized by progressive skeletal muscle degeneration.
38 a progressive and fatal genetic disorder of muscle degeneration.
39 -/- double mutants exhibit an early onset of muscle degeneration.
40 nts in IBM pathology and subsequent skeletal muscle degeneration.
41 ciated with muscle injury or disease-related muscle degeneration.
42 in chronic inflammation and severe skeletal muscle degeneration.
43 late inflammation, playing a central role in muscle degeneration across various disease contexts.
44 nclude that the early phase of infraspinatus muscle degeneration after tendon release involves the el
45 nd death of young men because of progressive muscle degeneration aggravated by sterile inflammation.
46 her therapies deal with secondary aspects of muscle degeneration, aiming, for example, at reducing in
47 l pathology is the earliest manifestation of muscle degeneration and a prominent characteristic of in
48 nteractions, giving rise to both progressive muscle degeneration and abnormal neuronal migration in t
50 with complement activity, leading to reduced muscle degeneration and augmented muscle function (P < 0
51 CTX)-mediated transient acute mouse model of muscle degeneration and compared the cardinal features w
52 muscle along with a significant decrease in muscle degeneration and concentrations of serum creatine
53 henotypes: decreased mobility, age-dependent muscle degeneration and defective photoreceptor path-fin
54 uced size, wobbly, waddling gait, along with muscle degeneration and dramatic reduction in skeletal m
55 These data demonstrate that, in addition to muscle degeneration and dystrophy, impaired neuromuscula
56 n deficiency causes muscle membrane lesions, muscle degeneration and eventually death in afflicted in
57 , triggered by NF-kappaB activation, promote muscle degeneration and failure of muscle regeneration.
60 -) background substantially reduced skeletal muscle degeneration and histopathology compared with the
61 RH2 mutation as a novel driver of congenital muscle degeneration and identifies a potential novel tar
64 tial for skeletal muscle regeneration, cause muscle degeneration and neuromuscular disease when mutat
66 ranscriptional alterations that occur during muscle degeneration and performed a genetic screen for p
67 VI-truncated laminin alpha2-chain results in muscle degeneration and peripheral nerve dysmyelination
70 eased slow fiber (type 1) density, increased muscle degeneration and regeneration in aged muscles, de
71 elop a progressive myopathy characterized by muscle degeneration and regeneration, and abnormal metab
72 owledge on FAP adipogenic differentiation in muscle degeneration and regeneration, with a focus on ca
77 Loss of gamma-sarcoglycan (gamma-SG) induces muscle degeneration and signaling defects in response to
79 es are characterized by distinct patterns of muscle degeneration and this helps in selecting other re
81 ive methods are available to assess RC fatty muscle degeneration and volume atrophy based on MRI.
83 essive disorder characterized by progressive muscle degeneration and weakness due to mutations in the
85 ide accumulation, mitochondrial dysfunction, muscle degeneration, and cardiac malfunction, which were
86 he relationship between IBM autoimmunity and muscle degeneration, and develop an IBM blood test with
87 lies are flightless, showing indirect flight muscle degeneration, and females are sterile, showing di
88 inery is responsible for dysferlin-deficient muscle degeneration, and highlight the importance of thi
89 ction resulting in male sterility, apoptotic muscle degeneration, and minor loss of dopamine neurons
90 epidermis, abnormal hair follicles, cardiac muscle degeneration, and reduced amount of collagen and
91 oss of luciferase expression associated with muscle degeneration, and that protection was enhanced by
93 y and the ability of the GnP matrix to treat muscle degeneration are promising for the realization of
95 phenotypes (fin erosion, cell apoptosis and muscle degeneration) are direct symptoms of infection.
97 -) mice exhibit differences in the extent of muscle degeneration between muscle groups with muscles e
98 Alendronate treatment did not ameliorate muscle degeneration, but demonstrated a limited enhancem
99 scle pathology with significant reduction in muscle degeneration, but had no effect on serum creatine
100 hallmarks of FSHD histopathology, including muscle degeneration, capillary loss, fibrosis, and atrop
101 en show cognitive impairment, in addition to muscle degeneration caused by dystrophin gene defects.
102 xpression of drp1, rescues the phenotypes of muscle degeneration, cell death, and mitochondrial abnor
105 NL3 activity in myogenic cells could lead to muscle degeneration disorders such as myotonic dystrophy
106 ing the progression of neurodegenerative and muscle degeneration disorders, the precise sequence of c
107 flammation of skeletal muscle and subsequent muscle degeneration due to an uncontrolled autoimmune re
108 phy (DMD) is a rare genetic disease, causing muscle degeneration due to lack of dystrophin with inade
109 Fatty expansion is one of the features of muscle degeneration due to muscle injuries, and its pres
110 genetic disease characterized by progressive muscle degeneration due to mutations in the dystrophin g
114 e loss of spinal cord motor neurons, reduces muscle degeneration, improves muscle fiber thickness and
118 is associated with swollen mitochondria and muscle degeneration in Drosophila melanogaster, as well
119 on substantially affect skeletal and cardiac muscle degeneration in Duchenne muscular dystrophy.
120 nctional, and metabolic changes conducive to muscle degeneration in Krabbe disease using the murine (
121 the importance of oxidative stress-mediated muscle degeneration in muscular dystrophy, and reveal th
122 o accelerate muscle regeneration and to slow muscle degeneration in myositis, focusing primarily on i
124 in this novel cell adhesion pathway, reduces muscle degeneration in zebrafish with intact integrin re
125 V treatment was safe, attenuated fibro-fatty muscle degeneration, increased myofiber size, and restor
127 ions in the dystrophin gene, involves severe muscle degeneration, inflammation, fibrosis, and early d
128 ouble-knockout strains displayed exacerbated muscle degeneration, inflammation, fibrosis, and reduced
131 dult myoblasts called satellite cells during muscle degeneration is an important aspect of muscle reg
133 DMD, we show here that dystrophin-dependent muscle degeneration is likely to be cell autonomous and
134 model of muscular dystrophy (mdx), in which muscle degeneration is rapidly followed by regeneration.
136 ly SMT C1100 treatment significantly reduced muscle degeneration leading to improved muscle function.
137 m in vivo and in vitro studies suggests that muscle degeneration may be secondary to an increased sus
138 alysis indicates that, prior to the onset of muscle degeneration, mutant muscles are hyperinnervated.
140 hogenesis suggests that at least part of the muscle degeneration observed in DMD patients may result
141 ibit different roles in dystrophin-dependent muscle degeneration occurring in a C. elegans model of D
143 es can take many forms, from the progressive muscle degeneration of dystrophies to the childhood canc
144 previous study showed that in the context of muscle degeneration on a mdx (dystrophin null) genetic b
148 risingly, we have found that the progressive muscle degeneration phenotype of sapje mutant zebrafish
149 emma integrity, observed at the onset of the muscle degeneration process, triggers subcellular conseq
150 ered position and size, vacuoli and signs of muscle degeneration-regeneration were observed in head,
153 ells activate and proliferate in response to muscle degeneration, resulting in an increase in the lev
156 omozygous mutants of tardbp and tardbpl show muscle degeneration, strongly reduced blood circulation,
158 arget CISD3 could therefore impact different muscle degeneration syndromes, aging, and related condit
160 trophy (DMD) is characterized by progressive muscle degeneration that results from the absence of dys
161 lycoprotein complex assembly, but to prevent muscle degeneration the expression of a functional dystr
162 in histopathology but ultimately exacerbates muscle degeneration; this effect was not observed in dys
164 ortant determinant of the severity of ageing muscle degeneration, we aimed to determine the presence
165 ential of targeting myostatin in settings of muscle degeneration, we crossed myostatin null mutant mi
166 cterized by progressive cardiac and skeletal muscle degeneration with childhood to adolescent onset.
167 Our analysis of drpr mutant flies revealed muscle degeneration with fiber size variability and vacu
168 scular disorder characterized by progressive muscle degeneration with substantial variability in seve