Skeletal Muscle Remodeling

2017 ◽  
Vol 45 (3) ◽  
pp. 187-191 ◽  
Author(s):  
Nicholas A. Burd ◽  
Michael De Lisio
2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Kunihiro Sakuma ◽  
Akihiko Yamaguchi

Skeletal muscle uses calcium as a second messenger to respond and adapt to environmental stimuli. Elevations in intracellular calcium levels activate calcineurin, a serine/threonine phosphatase, resulting in the expression of a set of genes involved in the maintenance, growth, and remodeling of skeletal muscle. In this review, we discuss the effects of calcineurin activity on hypertrophy, regeneration, and disorders of skeletal muscle. Calcineurin is a potent regulator of muscle remodeling, enhancing the differentiation through upregulation of myogenin or MEF2A and downregulation of the Id1 family and myostatin. Foxo may also be a downstream candidate for a calcineurin signaling molecule during muscle regeneration. The strategy of controlling the amount of calcineurin may be effective for the treatment of muscular disorders such as DMD, UCMD, and LGMD. Activation of calcineurin produces muscular hypertrophy of the slow-twitch soleus muscle but not fast-twitch muscles.


Author(s):  
T. O. Veresiuk ◽  
P. R. Selskyy ◽  
A. T. Televiak

Arterial tourniquets are used in clinical practice for angioplasty and arthroplasty, and in case of limb injuries, their use often occurs according to vital signs. After removing the tourniquet and blood supply restoration to the limb arises a multifactorial lesion of tissues both ischemic and distant from the site of ischemia. A number of publications have been devoted to the study of morphological disorders in muscle tissue in acute ischemia-reperfusion in the medical literature. However, the researches for effective means for drug correction of these disorders still continues. The aim of the study was to explore peculiarities of skeletal muscle remodeling of the hind limbs of rats, detected by polarization microscopy, in acute ischemia-reperfusion, caused by the application of an arterial tourniquet, and in the correction of reperfusion disorders by carbacetam. Microscopic examination of histological sections of skeletal muscles of the hind limbs of 60 rats below the site of application of the tourniquet under conditions of experimental acute ischemia-reperfusion was performed. Acute ischemia for all animals was caused by application of SWAT rubber bands on the hind limbs of animals, 5–6 mm in width, at the inguinal fold level within 2 hours under thiopental anesthesia. A reperfusion was modeled by removing the tourniquet. Half of the experimental animals in the reperfusion period for the purpose of correction intraperitoneally was administered the nootropic drug 1-oxo-3.3.6-trimethyl-1.2.3.4-tetrahydroindolo[2.3-c]quinoline (carbacetam) at a dose of 5 mg per kilogram of body weight once a day during the entire reperfusion period. The histological specimens of the skeletal muscles were stained with hematoxylin and eosin, and were examined with a light microscope with polarization nozzle. Studies with using the polarization microscopy have shown that in the early reperfusion period morphological criteria for skeletal muscle remodeling expressed by deformation and anisotropy of muscle fibers, disappearance of their transverse striation, cracks and ruptures of fibers, and in the most severe cases there were signs of necrosis of the fibers with their fragmentation into separate lumps. Subject to the correction of reperfusion disorders by carbacetam, there is a decrease in the degree of damage and consistent acceleration of restoration of the skeletal muscles structure, which was the most pronounced in groups of animals with reperfusion terms after 1 and 14 days. Complex of features indicates, that at the tissue level the administration of carbacetam as reduces the ischemic-reperfusion lesion of the muscular fibers, as also accelerates the mechanisms of reparative rhabdomyohistogenesis. Thus, structural changes in the skeletal muscles of the limb after two-hour ischemia and subsequent reperfusion increased in the early reperfusion period and reached its peak after 1 day of reperfusion, and in the late period of reperfusion their reverse development took place. With the correction of disorders by carbacetam, the degree of damage was reduced and the recovery of the skeletal muscle structure of the limb was accelerated.


2018 ◽  
Vol 11 (530) ◽  
pp. eaao6847 ◽  
Author(s):  
Jae-Sung You ◽  
Matthew S. Dooley ◽  
Chan-Ran Kim ◽  
Eui-Jun Kim ◽  
Wei Xu ◽  
...  

Author(s):  
Samuele Metti ◽  
Lisa Gambarotto ◽  
Martina Chrisam ◽  
Martina La Spina ◽  
Martina Baraldo ◽  
...  

The induction of autophagy, the catabolic pathway by which damaged or unnecessary cellular components are subjected to lysosome-mediated degradation and recycling, is impaired in Collagen VI (COL6) null mice and COL6-related myopathies. This autophagic impairment causes an accumulation of dysfunctional mitochondria, which in turn leads to myofiber degeneration. Our previous work showed that reactivation of autophagy in COL6-related myopathies is beneficial for muscle structure and function both in the animal model and in patients. Here we show that pterostilbene (Pt)—a non-toxic polyphenol, chemically similar to resveratrol but with a higher bioavailability and metabolic stability—strongly promotes in vivo autophagic flux in the skeletal muscle of both wild-type and COL6 null mice. Reactivation of autophagy in COL6-deficient muscles was also paralleled by several beneficial effects, including significantly decreased incidence of spontaneous apoptosis, recovery of ultrastructural defects and muscle remodeling. These findings point at Pt as an effective autophagy-inducing nutraceutical for skeletal muscle with great potential in counteracting the major pathogenic hallmarks of COL6-related myopathies, a valuable feature that may be also beneficial in other muscle pathologies characterized by defective regulation of the autophagic machinery.


Author(s):  
Mahavir Singh ◽  
Akash K George ◽  
Wintana Eyob ◽  
Rubens Petit Homme ◽  
Dragana Stanisic ◽  
...  

Epigenetic DNA methylation is crucial for gene-imprinting/off-printing ensuring epigenetic memory but generates copious homocysteine (Hcy) unequivocally. That is why during pregnancy mothers are recommended ‘folic acid’ to avoid birth-defects because of elevated Hcy levels (hyperhomocysteinemia; HHcy). Children born with HHcy have musculoskeletal abnormalities/growth retardation. We focus on gut-dysbiotic microbiome implication that instigates “1-carbon metabolism” and HHcy causing growth retardation along with muscle abnormalities. We test hypothesis whether high methionine diet (HMD, an amino acid high in red-meat) a substrate for Hcy can cause skeletal muscle and growth retardation and treatment with probiotics (PB) mitigate muscle dysfunction. We employed cystathionine beta synthase; CBS deficient mouse; CBS+/- fed with/without HMD and with/without a probiotic in drinking water for 16 weeks. Matrix metalloproteinase activity; a hallmark of remodeling was measured by zymography. Muscle functions were scored via electric stimulation. Our results suggest that compared to WT, CBS+/- mice exhibited reduced growth. MMP-2 activity was robust in CBS+/- and HMD effects were attenuated by PB intervention. Electrical stimulation magnitude was decreased in CBS+/- and CBS+/- treated with HMD. Interestingly; PB mitigated muscle growth retardation and atrophy. Collectively, results imply that individuals with mild/moderate HHcy seem more prone to skeletal muscle injury and its dysfunction


2012 ◽  
Vol 17 (6) ◽  
pp. 693-705 ◽  
Author(s):  
Chad D. Touchberry ◽  
Anisha A. Gupte ◽  
Gregory L. Bomhoff ◽  
Zachary A. Graham ◽  
Paige C. Geiger ◽  
...  

2008 ◽  
Vol 33 (6) ◽  
pp. 1181-1191 ◽  
Author(s):  
Brent A. Baker ◽  
Melinda S. Hollander ◽  
Robert R. Mercer ◽  
Michael L. Kashon ◽  
Robert G. Cutlip

This study determined the age-related changes in acute events responsible for initiating skeletal muscle remodeling and (or) regeneration in the tibialis anterior muscle following a bout of stretch-shortening contractions (SSCs). Changes in muscle performance and morphology were quantified in young and old rats, following an acute exposure to adaptive SSCs at 6, 24, 48, 72, and 120 h postexposure (n = 6 for each age at each recovery period). Following SSC exposure, all performance measures were decreased in old rats throughout the 120 h acute phase. Estimates of edema were increased in the old vs. young exposed muscle at 120 h recovery. Both young and old rats displayed an increase in developmental myosin heavy chain (MHCdev+) labeling in the exposed muscle, indicating muscle regeneration. However, old rats displayed diminished MHCdev+ labeling, compared with young rats, suggesting limited remodeling and (or) regenerative capacity. Based on these data, diminished local muscle remodeling and (or) regeneration with aging may limit skeletal muscle adaptation following mechanical loading.


2003 ◽  
Vol 41 (6) ◽  
pp. 168
Author(s):  
Erik J. Kouba ◽  
Gregory Hundley ◽  
Peter Brubaker ◽  
Barbara Nicklas ◽  
Dalane W. Kitzman

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