Faculty Opinions recommendation of Loss of the inducible Hsp70 delays the inflammatory response to skeletal muscle injury and severely impairs muscle regeneration.

Author(s):  
Michael Tytell ◽  
Mac Robinson
PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e62687 ◽  
Author(s):  
Sarah M. Senf ◽  
Travis M. Howard ◽  
Bumsoo Ahn ◽  
Leonardo F. Ferreira ◽  
Andrew R. Judge

2013 ◽  
Vol 115 (6) ◽  
pp. 920-928 ◽  
Author(s):  
Maria L. Urso

Exercise, eccentric contractions, acute trauma, and disease are all causal mechanisms of skeletal muscle injury. After skeletal muscle is injured, it undergoes sequential phases of degeneration, inflammation, regeneration, and fibrosis. Events that occur in response to inflammation trigger regenerative processes. However, since inflammation causes pain, decreases skeletal muscle function, has a negative effect on performance, and contributes to fibrosis, which is one of the leading causes of delayed regeneration, the general practice has been to reduce inflammation. The problem with this approach is that preventing inflammation may hinder recovery. Current treatment options for inflammation are not necessarily effective and, in some cases, they may be unsafe. This review focuses on the question of whether the most beneficial course of treatment should be to block inflammation or if it is sensible to allow inflammatory processes to progress naturally. If blocking inflammation is perceived as a beneficial approach, it is not yet known at what time point during the inflammatory response it is most sensible to interfere. To address these issues, this review evaluates the effects of various anti-inflammatory agents on recovery processes in response to exercise-induced, traumatic, and disease-associated models of skeletal muscle injury. A collective analysis such as this should lay the foundation for future work that systematically manipulates the inflammatory response to most effectively promote regeneration and functional recovery in injured skeletal muscle, while reducing the negative effects of inflammatory processes such as pain and fibrosis.


Phytomedicine ◽  
2021 ◽  
pp. 153791
Author(s):  
Maria Sikorska ◽  
Małgorzata Dutkiewicz ◽  
Oliwia Zegrocka – Stendel ◽  
Magdalena Kowalewska ◽  
Iwona Grabowska ◽  
...  

2016 ◽  
Vol 4 ◽  
pp. 1-10 ◽  
Author(s):  
Hongxue Shi ◽  
Haohuang Xie ◽  
Yan Zhao ◽  
Cai Lin ◽  
Feifei Cui ◽  
...  

Abstract Background Pressure ulcers (PUs) are a major clinical problem that constitutes a tremendous economic burden on healthcare systems. Deep tissue injury (DTI) is a unique serious type of pressure ulcer that arises in skeletal muscle tissue. DTI arises in part because skeletal muscle tissues are more susceptible than skin to external compression. Unfortunately, few effective therapies are currently available for muscle injury. Basic fibroblast growth factor (bFGF), a potent mitogen and survival factor for various cells, plays a crucial role in the regulation of muscle development and homeostasis. The main purpose of this study was to test whether local administration of bFGF could accelerate muscle regeneration in a rat DTI model. Methods Male Sprague Dawley (SD) rats (age 12 weeks) were individually housed in plastic cages and a DTI PU model was induced according to methods described before. Animals were randomly divided into three groups: a normal group, a PU group treated with saline, and a PU group treated with bFGF (10 μg/0.1 ml) subcutaneously near the wound. Results We found that application of bFGF accelerated the rate of wound closure and promoted cell proliferation and tissue angiogenesis. In addition, compared to saline administration, bFGF treatment prevented collagen deposition, a measure of fibrosis, and up-regulated the myogenic marker proteins MyHC and myogenin, suggesting bFGF promoted injured muscle regeneration. Moreover, bFGF treatment increased levels of myogenesis-related proteins p-Akt and p-mTOR. Conclusions Our findings show that bFGF accelerated injured skeletal muscle regeneration through activation of the PI3K/Akt/mTOR signaling pathway and suggest that administration of bFGF is a potential therapeutic strategy for the treatment of skeletal muscle injury in PUs.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Ya Tan ◽  
Linyuan Shen ◽  
Mailin Gan ◽  
Yuan Fan ◽  
Xiao Cheng ◽  
...  

Skeletal muscle is the most abundant and a highly plastic tissue of the mammals, especially when it comes to regenerate after trauma, but there is limited information about the mechanism of muscle repair and its regeneration. In the present study, we found that miR-204 is downregulated after skeletal muscle injury. In vitro experiments showed that over-expression of miR-204 by transfecting with miR-204 mimics suppressed C2C12 cell proliferation, migration, and blocked subsequent differentiation, whereas inhibition of miR-204 by transfecting with miR-204 inhibitor showed the converse effects. Furthermore, through the dual luciferase reporter system, we demonstrated that miR-204 can target the 3’UTR regions of Pax7, IGF1, and Mef2c and inhibit their expression. Taken together, our results suggest that Pax7, IGF1, and Mef2c are the target genes of miR-204 in the process of myoblasts proliferation, cell migration, and differentiation, respectively, and may contribute to mouse skeletal muscle regeneration. Our results may provide new ideas and references for the skeletal muscle study and may also provide therapeutic strategies of skeletal muscle injury.


2021 ◽  
Author(s):  
Jonas Brorson Jensen ◽  
Ole Lindgaard Dollerup ◽  
Andreas Buch Moeller ◽  
Tine Borum Billeskov ◽  
Emilie Dalbram ◽  
...  

Background Maintenance and regeneration of functional skeletal muscle are dependent on a sufficient pool of muscle stem cells (MuSCs). During ageing there is a functional decline in this cellular pool which influences the regenerative capacity of skeletal muscle. Preclinical evidence have suggested that Nicotinamide Riboside (NR) and Pterostilbene (PT) can improve muscle regeneration e.g. by increasing MuSC function. The objective of the present study was to investigate if NRPT supplementation promotes skeletal muscle regeneration after muscle injury in elderly humans by improved recruitment of MuSCs. Methods In a randomized, double-blinded, placebo-controlled trial, 32 elderly men and women (55-80 yr) received daily supplementation with either NRPT (1000 mg NR + 200 mg PT) or matched placebo. Two weeks after initiation of supplementation, a skeletal muscle injury was applied in the vastus lateralis part of the quadriceps femoris muscle by electrically induced eccentric muscle work in a dynamometer. Skeletal muscle biopsies were obtained pre, 2h, 2, 8, and 30 days post injury. The main outcome of the study was change in MuSC content 8 days post injury. Results 31 enrolled subjects completed the entire protocol. The muscle work induced a substantial skeletal muscle injury in the study participants and was associated with release of myoglobin and creatine kinase, muscle soreness, tissue edema, and a decrease in muscle strength. MuSC content increased by 107% 8 days post injury (p= 0.0002) but with no effect of NRPT supplementation (p=0.58 for supplementation effect). MuSC proliferation and cell size revealed a large demand for recruitment post injury but was not affected by NRPT. Furthermore, histological analyses of muscle fiber area, internal nuclei and embryonic Myosin Heavy Chain showed no effect of NRPT supplementation. Conclusion Daily supplementation with 1000 mg NR + 200 mg PT is safe but does not improve recruitment of the MuSC pool or other measures of muscle recovery in response to injury or subsequent regeneration in elderly subjects.


2009 ◽  
Vol 14 (10) ◽  
pp. 2495-2505 ◽  
Author(s):  
Tomoyuki Nakasa ◽  
Masakazu Ishikawa ◽  
Ming Shi ◽  
Hayatoshi Shibuya ◽  
Nobuo Adachi ◽  
...  

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