Transforming growth factor-?2 is elevated in skeletal muscle disorders

1999 ◽  
Vol 22 (7) ◽  
pp. 889-898 ◽  
Author(s):  
Nobuyuki Murakami ◽  
Ian S. McLennan ◽  
Ikuya Nonaka ◽  
Kyoko Koishi ◽  
Christina Baker ◽  
...  
2003 ◽  
Vol 95 (2) ◽  
pp. 771-780 ◽  
Author(s):  
Yi-Sheng Chan ◽  
Yong Li ◽  
William Foster ◽  
Takashi Horaguchi ◽  
George Somogyi ◽  
...  

Muscle injuries are very common in traumatology and sports medicine. Although muscle tissue can regenerate postinjury, the healing process is slow and often incomplete; complete recovery after skeletal muscle injury is hindered by fibrosis. Our studies have shown that decreased fibrosis could improve muscle healing. Suramin has been found to inhibit transforming growth factor (TGF)-β1 expression by competitively binding to the growth factor receptor. We conducted a series of tests to determine the antifibrotic effects of suramin on muscle laceration injuries. Our results demonstrate that suramin (50 μg/ml) can effectively decrease fibroblast proliferation and fibrotic-protein expression (α-smooth muscle actin) in vitro. In vivo, direct injection of suramin (2.5 mg) into injured murine muscle resulted in effective inhibition of muscle fibrosis and enhanced muscle regeneration, which led to efficient functional muscle recovery. These results support our hypothesis that prevention of fibrosis could enhance muscle regeneration, thereby facilitating more efficient muscle healing. This study could significantly contribute to the development of strategies to promote efficient muscle healing and functional recovery.


1988 ◽  
Vol 34 (12) ◽  
pp. 2460-2462 ◽  
Author(s):  
J Arenas ◽  
V Diaz ◽  
G Liras ◽  
E Gutierrez ◽  
I Santos ◽  
...  

Abstract We studied possible correlations between anatomopathological and clinical features and the values for total creatine kinase (CK; EC 2.7.3.2) and its isoenzymes, including the proportion of CK-MB, in a population displaying several neuromuscular pathologies. Although we observed no specific isoenzyme pattern associated with the different myopathies, we found isoenzyme analysis useful in studying the histopathological evolution of illness. We also considered whether the pathology was regenerative or nonregenerative, and what type of fiber (I or II) was involved. High CK-MB percentages (greater than 6%) were associated with regenerative and type I fiber myopathies, with regenerative type tissues being the principal factor associated with an increasing proportion of CK-MB. Studying the changes in CK-MB percentage in serum appears to be useful in discriminating neuromuscular from myocardial pathologies.


2020 ◽  
Vol 7 (3) ◽  
pp. 203-216 ◽  
Author(s):  
Marco Savarese ◽  
Salla Välipakka ◽  
Mridul Johari ◽  
Peter Hackman ◽  
Bjarne Udd

Muscle ◽  
2012 ◽  
pp. 1045-1051 ◽  
Author(s):  
Andrea L.H. Arnett ◽  
Julian N. Ramos ◽  
Jeffrey S. Chamberlain

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 288 ◽  
Author(s):  
Alessandra Stacchiotti ◽  
Gaia Favero ◽  
Luigi Fabrizio Rodella

Skeletal muscle disorders are dramatically increasing with human aging with enormous sanitary costs and impact on the quality of life. Preventive and therapeutic tools to limit onset and progression of muscle frailty include nutrition and physical training. Melatonin, the indole produced at nighttime in pineal and extra-pineal sites in mammalians, has recognized anti-aging, anti-inflammatory, and anti-oxidant properties. Mitochondria are the favorite target of melatonin, which maintains them efficiently, scavenging free radicals and reducing oxidative damage. Here, we discuss the most recent evidence of dietary melatonin efficacy in age-related skeletal muscle disorders in cellular, preclinical, and clinical studies. Furthermore, we analyze the emerging impact of melatonin on physical activity. Finally, we consider the newest evidence of the gut–muscle axis and the influence of exercise and probably melatonin on the microbiota. In our opinion, this review reinforces the relevance of melatonin as a safe nutraceutical that limits skeletal muscle frailty and prolongs physical performance.


2001 ◽  
Vol 33 (5) ◽  
pp. S230 ◽  
Author(s):  
C A. Smith ◽  
W T. Stauber, FACSM ◽  
S E. Alway, FACSM ◽  
G R. Miller

2008 ◽  
Vol 104 (3) ◽  
pp. 579-587 ◽  
Author(s):  
Helen D. Kollias ◽  
John C. McDermott

The superfamily of transforming growth factor-β (TGF-β) cytokines has been shown to have profound effects on cellular proliferation, differentiation, and growth. Recently, there have been major advances in our understanding of the signaling pathway(s) conveying TGF-β signals to the nucleus to ultimately control gene expression. One tissue that is potently influenced by TGF-β superfamily signaling is skeletal muscle. Skeletal muscle ontogeny and postnatal physiology have proven to be exquisitely sensitive to the TGF-β superfamily cytokine milieu in various animal systems from mice to humans. Recently, major strides have been made in understanding the role of TGF-β and its closely related family member, myostatin, in these processes. In this overview, we will review recent advances in our understanding of the TGF-β and myostatin signaling pathways and, in particular, focus on the implications of this signaling pathway for skeletal muscle development, physiology, and pathology.


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