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1 ctility despite a lack of effect on skeletal muscle hypertrophy.
2 ht to be a critical step in the induction of muscle hypertrophy.
3 s that contribute to hypertension and smooth muscle hypertrophy.
4 ce the pathways normally leading to skeletal muscle hypertrophy.
5 ber-type switching, and cardiac and skeletal muscle hypertrophy.
6 ack of glycolytic fibers as well as signs of muscle hypertrophy.
7 g in coordinating angiogenesis with skeletal muscle hypertrophy.
8 ntially expressed mRNA during early skeletal muscle hypertrophy.
9 nterior (TA) muscle has been shown to elicit muscle hypertrophy.
10 hypothesize that it plays a role in skeletal muscle hypertrophy.
11 additional signals are required for skeletal muscle hypertrophy.
12  muscle fibers, but no evidence for skeletal muscle hypertrophy.
13 s, and fibrosis, as well as oviductal smooth muscle hypertrophy.
14 ctivating mutations of myostatin have marked muscle hypertrophy.
15  between measures used to assess RET-induced muscle hypertrophy.
16 n resistance exercise training (RET)-induced muscle hypertrophy.
17 nd normal eye (p-value = 0.90) with Muller's muscle hypertrophy.
18 ell as impairment of mechanical load-induced muscle hypertrophy.
19 skeletal muscle to test whether they induced muscle hypertrophy.
20 igenetic memory of exercise induced skeletal muscle hypertrophy.
21 tion throughout the protocol, and functional muscle hypertrophy.
22 R signaling, protein synthesis, and skeletal muscle hypertrophy.
23  stem cell fusion during physiological adult muscle hypertrophy.
24 nse relationship between training volume and muscle hypertrophy.
25 king ribosome biogenesis central to skeletal muscle hypertrophy.
26 PGC1alpha mRNA and has been shown to promote muscle hypertrophy.
27 mass, while deletion of Tp53inp2 resulted in muscle hypertrophy.
28 t is unrelated to mucus metaplasia or smooth muscle hypertrophy.
29 in vitro and in vivo induces robust skeletal muscle hypertrophy.
30 fically in myofibers is sufficient to induce muscle hypertrophy.
31 and coordinates factors involved in skeletal muscle hypertrophy.
32  Cripto accelerates regeneration, leading to muscle hypertrophy.
33 at ActRIIB inhibition results in significant muscle hypertrophy.
34  during mechanical overload-induced skeletal muscle hypertrophy.
35 chanism and is sufficient to induce skeletal muscle hypertrophy.
36 rmal kidney function exhibited mild skeletal muscle hypertrophy.
37 and sufficient for the induction of skeletal muscle hypertrophy.
38 n, whether mainly inflammation, fibrosis, or muscle hypertrophy.
39 ixed findings of inflammation, fibrosis, and muscle hypertrophy.
40 fibroblasts to stimulate myoblast fusion and muscle hypertrophy.
41  prolong mTORC1 signalling and contribute to muscle hypertrophy.
42 equired for GSK-3beta-mediated airway smooth muscle hypertrophy.
43 ons and measure wasting and exercise-induced muscle hypertrophy.
44 c subtype (inflammation, 5; fibrosis, 4; and muscle hypertrophy, 3), acute and chronic inflammation,
45 beta (GSK-3beta) inhibition in airway smooth muscle hypertrophy, a structural change found in patient
46    Here, we show that loss of Raptor reduces muscle hypertrophy after Akt activation and completely p
47                       Moreover, we show that muscle hypertrophy after pharmacological blockade of thi
48 indicate that work overload induced skeletal muscle hypertrophy alters autocrine/paracrine signaling,
49 lly significant association between Muller's muscle hypertrophy and 1 mm correction effect, ptosis co
50  characterized by the inability to walk, leg muscle hypertrophy and a secondary deficiency of laminin
51 ur results confirm that HP diets can augment muscle hypertrophy and accelerate strength gain induced
52 st that increased mechanical load can induce muscle hypertrophy and activate the Akt and p70(s6k) ind
53 GPR56 expression attenuates overload-induced muscle hypertrophy and associated anabolic signaling.
54 d unexpectedly myostatin, known mediators of muscle hypertrophy and atrophy, respectively.
55 ing the complex molecular systems underlying muscle hypertrophy and atrophy.
56  delivered IGF-1 genes induce local skeletal muscle hypertrophy and attenuate age-related skeletal mu
57    As rapamycin can attenuate bladder smooth muscle hypertrophy and dysfunction during the genesis of
58 amycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effect
59 xercise on metabolic health and particularly muscle hypertrophy and fat loss are well established, bu
60 hat alpha-ketoglutaric acid (AKG) stimulates muscle hypertrophy and fat loss through 2-oxoglutarate r
61  derived molecule for adrenal stimulation of muscle hypertrophy and fat loss.
62 t cell hyperplasia and metaplasia and smooth muscle hypertrophy and fibrosis); levels of IgE, eotaxin
63 f (18)F-FDG PET/CT for differentiating fixed muscle hypertrophy and fibrotic stenoses from acute tran
64  top of GDF8 inhibition, leads to pronounced muscle hypertrophy and force production in mice and monk
65 r fasting or denervation without stimulating muscle hypertrophy and GHSR-1a-mediated activation of th
66 odulated PTEN/AKT signaling, which regulates muscle hypertrophy and growth, and induced apoptosis.
67 ed evidence of significant intestinal smooth muscle hypertrophy and hyperplasia associated with abnor
68 fibrosis, goblet cell metaplasia, and smooth muscle hypertrophy and hyperplasia).
69 es GATOR1 inhibition of mTORC1, resulting in muscle hypertrophy and increased mitochondrial respirati
70                     CTRND05 induces skeletal muscle hypertrophy and increases lean body mass, effects
71 Vector treatment also prevented pathological muscle hypertrophy and resulted in normal muscle weight
72 , thirteen displayed clear benefit of MOD on muscle hypertrophy and sixteen showed clear benefit of M
73 idence that endurance exercise can attenuate muscle hypertrophy and strength but the mechanistic unde
74 splayed clear benefits in response to MOD on muscle hypertrophy and strength.
75 ting Akt will be useful in inducing skeletal muscle hypertrophy and that an increase in lean muscle m
76 n of extracellular matrix components, smooth muscle hypertrophy and thickening of the lamina reticula
77 se in mechanical loading can induce skeletal muscle hypertrophy, and a long standing model in the fie
78 ID1 and TSLP, inflammation, fibrosis, smooth muscle hypertrophy, and expression of inflammatory effec
79 arts exhibited atrial enlargement, papillary muscle hypertrophy, and fibrosis.
80 eness, atherosclerosis, angiogenesis, smooth muscle hypertrophy, and hyperplasia.
81 e satellite cell (SC) response to RT-induced muscle hypertrophy, and hypothesized that aerobic condit
82 skeletal muscle atrophy, stimulated skeletal muscle hypertrophy, and increased strength and exercise
83 nd to enhance alpha7 integrin levels, induce muscle hypertrophy, and inhibit apoptosis in myotubes by
84              Similar FFM accretion, skeletal muscle hypertrophy, and muscular performance improvement
85 re all positively correlated with percentage muscle hypertrophy, and negatively correlated with the p
86 esponsiveness, mucus cell metaplasia, smooth muscle hypertrophy, and subepithelial fibrosis.
87 naling pathway through GPR56 which regulates muscle hypertrophy associated with resistance/loading-ty
88 at it contributes to mechanical load-induced muscle hypertrophy, at least in part by mediating signal
89 ude bronchial wall thickening, airway smooth muscle hypertrophy, bronchiectasis and emphysema.
90 logical elevation of circulating AKG induces muscle hypertrophy, brown adipose tissue (BAT) thermogen
91 tor PGC-1alpha) expression not only promotes muscle hypertrophy but also enhances glycolysis, providi
92 kly training (3x/week vs. 2x/week) increases muscle hypertrophy but not maximal dynamic strength.
93                     mTORC1 promotes skeletal muscle hypertrophy, but also drives organismal aging.
94 like growth factor 1 (IGF1) induces skeletal muscle hypertrophy by activating the IGF1R/IRS1/PI3K/Akt
95 t depending on the disease context, inducing muscle hypertrophy by myostatin blockade may have detrim
96 unctional overload model to induce plantaris muscle hypertrophy by surgically removing the soleus and
97                To evaluate whether promoting muscle hypertrophy can attenuate symptoms resulting from
98 hed model of pressure overload-induced heart muscle hypertrophy caused by transverse aortic constrict
99 ported that growth promoter-induced skeletal muscle hypertrophy co-ordinately upregulated expression
100                                              Muscle hypertrophy coincided with significant elevations
101                    Promoting skeletal muscle muscle hypertrophy could therefore have potential applic
102 and molecular mechanisms underlying skeletal muscle hypertrophy, expression profiles of translational
103  in hypertrophic responses, we observed that muscle hypertrophy following RET was relatively well con
104 gate how AC alters SC content, activity, and muscle hypertrophy following RT.
105 lthough the molecular mechanism for skeletal muscle hypertrophy has been well studied, it still is no
106 he significance of this process during adult muscle hypertrophy has not been explored.
107 nt of how mechanistic research into skeletal muscle hypertrophy has progressed.
108 erlying mechanical overload-induced skeletal muscle hypertrophy have been extensively researched sinc
109 ling in C3KO muscles resulted in significant muscle hypertrophy; however, there were no improvements
110 and epithelium, diminished intestinal smooth muscle hypertrophy/hyperplasia, and impaired worm expuls
111 bservation that loss of myostatin results in muscle hypertrophy in a human subject.
112 g a miRNA-based mechanism that could explain muscle hypertrophy in human lipodystrophy.
113 erved, potent negative regulator of skeletal muscle hypertrophy in many species, from rodents to huma
114 hat myostatin/activin A inhibition can cause muscle hypertrophy in mice lacking either syndecan4 or P
115 e S6K-S6 axis in skeletal muscle and induced muscle hypertrophy in mice.
116 to challenge in G allele carriers, promoting muscle hypertrophy in normal females, but increased dama
117  whole body protein metabolism or RT-induced muscle hypertrophy in older people.
118 e myogenesis in non-muscle cells, to promote muscle hypertrophy in postnatal mice, and to activate tr
119                                              Muscle hypertrophy in response to increasing demand is d
120 umption by older people may promote skeletal muscle hypertrophy in response to resistance training (R
121 owth factor (IGF) system in exercise-induced muscle hypertrophy in the context of RA.
122 inflammation, collagen deposition and smooth muscle hypertrophy in the lungs of a murine model of ova
123 CA inhibitor, was able to prevent and reduce muscle hypertrophy in the mouse model with correction of
124         To understand the physiopathology of muscle hypertrophy in this context, we created a mouse m
125 control pathway contributes to airway smooth muscle hypertrophy in vitro and in vivo.
126 down of GPR56 attenuates PGC-1alpha4-induced muscle hypertrophy in vitro.
127 itro In mice, knockdown of AK017368 promoted muscle hypertrophy in vivo RNA molecules of AK017368 act
128 ent to induce rapid and significant skeletal muscle hypertrophy in vivo, accompanied by activation of
129                               Interestingly, muscle hypertrophy increased the transport of high molec
130 bronchial fibrosis, and peribronchial smooth muscle hypertrophy; increased levels of interleukin (IL)
131 ng the beta2-AR pathway can promote skeletal muscle hypertrophy independent of ligand administration,
132 s develop a spontaneous cardiac and skeletal muscle hypertrophy, indicating cooperative control of mu
133 and the role of satellite cells in mediating muscle hypertrophy induced by inhibition of this signali
134                        Our data suggest that muscle hypertrophy, induced by myostatin inhibition, lea
135           A murine model of overload-induced muscle hypertrophy is associated with increased expressi
136                                Airway smooth muscle hypertrophy is one of the hallmarks of airway rem
137         However we observed that RET-induced muscle hypertrophy is relatively conserved within an ind
138  list of mechanisms associated with skeletal muscle hypertrophy is then outlined, and areas of disagr
139        The mechanism linking the mutation to muscle hypertrophy is unclear but involves DLK1 overexpr
140                                  In skeletal muscle, hypertrophy is generally regarded as a beneficia
141  fibrosis (median, 50%; range, 40%-90%), and muscle hypertrophy (median, 20-fold thickening; range, 9
142    No patient with predominantly fibrosis or muscle hypertrophy (n = 7) had an SUL(max) greater than
143 -PDK1KO mice, suggesting that PDK1 regulates muscle hypertrophy not through changes in gene expressio
144 +2% to 3% relative to baseline) and skeletal muscle hypertrophy occurred in all groups.
145                     Variation in RET-induced muscle hypertrophy occurred independent of external load
146 elial cell proliferation and vascular smooth muscle hypertrophy of the small precapillary pulmonary a
147 ophy; and 3) identified secondary effects of muscle hypertrophy on body composition.
148           Mutations in MSTN gene can lead to muscle hypertrophy or double-muscled (DM) phenotype in c
149 ot show a significant difference in skeletal muscle hypertrophy or strength with resistance training.
150  is used to treat conditions associated with muscle hypertrophy or to enhance muscle flexibility, the
151 ular myocilin plays a role as a regulator of muscle hypertrophy pathways, acting through the componen
152  to carry the mutation causing the callipyge muscle hypertrophy phenotype in sheep.
153  in Marchigiana cattle, a breed in which the muscle hypertrophy phenotype is segregating.
154                              Coinciding with muscle hypertrophy, previously diminished muscle levels
155 ated the role of Myocilin (Myoc), a skeletal muscle hypertrophy-promoting protein that we showed is d
156 s that provide the extra nuclei required for muscle hypertrophy, repair and maintenance.
157 mber of muscle groups trained influenced the muscle hypertrophy response to RT.
158                                     Skeletal muscle hypertrophy stimulated by clenbuterol, a beta2-ad
159          NSAID intervention produced greater muscle hypertrophy than PLA, which occurred between 28 a
160                                    Papillary muscle hypertrophy that produced midcavitary obstruction
161 ks prior to denervation or tenotomy promoted muscle hypertrophy that was sufficient to preserve muscl
162 xtensive evidence implicating Ras in cardiac muscle hypertrophy, the mechanisms involved are unclear.
163 t satellite cells are necessary for skeletal muscle hypertrophy, the plantaris muscle of adult Pax7-D
164                                  Generalized muscle hypertrophy, transient weakness and depressed ten
165  the C-terminus is reported to contribute to muscle hypertrophy via the IGF-1 growth pathway.
166                    For mdx mice of all ages, muscle hypertrophy was highly effective in the maintenan
167                                     Skeletal muscle hypertrophy was induced in the plantaris muscle u
168                                              Muscle hypertrophy was initiated by bilateral ablation o
169  the IGF-I receptor in load-induced skeletal muscle hypertrophy, we utilized a transgenic mouse model
170 ad-induced activation of the S6K-S6 axis and muscle hypertrophy were inhibited in mice with skeletal
171 uced increases in contractility and skeletal muscle hypertrophy were lost in beta-arrestin 1 knockout
172 taplasia, peribronchial fibrosis, and smooth muscle hypertrophy were quantitated on tissue sections.
173 y (via DNA methylation) after human skeletal muscle hypertrophy, where its gene expression is positiv
174 d activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-AT
175  and may behave as a key modulator of smooth muscle hypertrophy, which is relevant for organ remodeli
176 ndividuals have a reduced capacity to induce muscle hypertrophy with resistance exercise (RE), which
177 udy, we; 1) characterized the development of muscle hypertrophy with respect to fiber type, age, and
178 was that strength training, which stimulates muscle hypertrophy, would help preserve both FFM and RMR

 
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