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Muscle Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Kourosh Rezania, Peter Pytel, Betty Soliven
Others: Utrophin is a protein that is expressed at neuromuscular and musculotendinous junctions. It shows homology to dystrophin. Upregulation of utrophin may be able to compensate for some of the effects of dystrophin loss.Inducing muscle hypertrophy by upregulating genes involved in muscle growth, such as insulin-like growth factor 1 (IGF-1) or L-arginine, may help to fight muscle wasting.Blocking the effect of myostatin as a negative regulator of muscle mass could have a similar beneficial effect.
Adipose Tissue (Adipokinome), Skeletal Muscle (Myokinome), and Liver (Hepatokinome) as Endocrine Regulators During Exercise
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Logan K. Townsend, Greg L. McKie, Hesham Shamshoum, David C. Wright
Myostatin is one of the only myokines that is reduced in response to exercise (84). Myostatin inhibits muscle cell proliferation and differentiation via an autocrine and paracrine mechanism. The genetic deletion of myostatin leads to muscle hypertrophy in mice and humans (74, 84, 115, 122). Myostatin inhibition positively regulates muscle growth, and myostatin expression is down-regulated after endurance and resistance exercise (1). Therefore, it has been proposed that myostatin inhibition could serve as a therapeutic agent for treatment of patients with muscular dystrophies (71). Myostatin has also been suggested to be a negative regulator of glucose and lipid metabolism (32, 39, 147). In high-fat diet-fed mice, it has been shown that inhibition of myostatin ameliorates obesity and the development of insulin resistance, and this associates with increases in the browning of white adipose tissue (145).
Chicken Eggs and Human Health
Published in Robert E.C. Wildman, Richard S. Bruno, Handbook of Nutraceuticals and Functional Foods, 2019
Jonathan Merkle, Christopher Bailey, Kevin Ruff
Recently, a new nutraceutical ingredient has been marked for enhancing strength and lean muscle mass. Derived from fertilized egg yolks, preliminary research in rats demonstrated that exercise combined with fertilized egg yolk isolate supplementation significantly reduced activin IIB receptor mRNA (p < 0.05), suggesting an inhibitory effect on the myostatin pathway.75 Myostatin signaling occurs through activin type II receptors.76 Myostatin has an inhibitory or limiting effect on muscle mass.76 Inhibition of this pathway has gained popularity as a target for increasing muscle mass as a result of the “double-muscled” appearance of some animals that have had genetic mutations in the coding sequence of myostatin, such as the Belgian Blue and Piedmontese cattle breeds.77
Insight into the role of myokines and myogenic regulatory factors under hypobaric hypoxia induced skeletal muscle loss
Published in Biomarkers, 2022
Sukanya Srivastava, Richa Rathor, Som Nath Singh, Geetha Suryakumar
In the present study, the proteins which regulate the myogenesis and energy metabolism in the skeletal muscle under HH stress were uploaded into the STRING software 11.5v to investigate the interactions among them (Figure 6). The confidence of score generated via software was used to establish protein–protein interaction. According to STRING 11.5v software, 0.150 score for low, 0.400 score for medium, 0.700 score for high and 0.900 score for the highest confidence respectively. The score among all the proteins is presented on Table 1. Total of 17 proteins were taken to perform string analysis. Out of which on the basis of scores and interaction Smad3, Smad4, Foxo1, Sirt1, Mstn, Ppargc1a, Myod1, Pax7, Myog, Prkaa2, Il6, Trim63, Il15 and Ccnd1 showed high and highest confidence. Amongst the proteins analysed, Mstn was found to have interaction with all the proteins validated in the study. These results indicate the role of myostatin in regulating the key proteins involving myogenesis, muscle regeneration and protein degradation.
Proteomic serum biomarkers for neuromuscular diseases
Published in Expert Review of Proteomics, 2018
Sandra Murphy, Margit Zweyer, Rustam R. Mundegar, Dieter Swandulla, Kay Ohlendieck
Unfortunately, many of the identified serum proteins that correlate with sarcopenia or frailty are not highly specific, making differential diagnostic evaluations difficult. For example, altered levels of serum myostatin were also shown to occur in several genetic muscle diseases that are unrelated to the natural aging process. Myostatin acts as a major negative regulator of skeletal muscle mass and growth, suggesting that the pharmacological inhibition of myostatin action may be an effective countermeasure to treat sarcopenia [89] and other neuromuscular disorders [90]. Besides in sarcopenia, decreased serum myostatin concentration has also been described to occur in several types of inherited muscular dystrophy [91], as discussed in more detail in the following section. Increased myostatin levels were found in serum specimens from Pompe disease patients receiving enzyme replacement therapy [92]. Pompe disease is a lysosomal glycogen storage disorder that is triggered by deficiency in acid α-glucosidase that particularly affects skeletal muscles.
Therapeutic interventions for spinal muscular atrophy: preclinical and early clinical development opportunities
Published in Expert Opinion on Investigational Drugs, 2021
Laurent Servais, Giovanni Baranello, Mariacristina Scoto, Aurore Daron, Maryam Oskoui
Myostatin inhibition is a relatively recent therapeutic approach for treatment of SMA that is based on the possibility that motor function in SMA patients could be additionally improved by targeting skeletal muscle to reduce atrophy and improve muscle strength. Myostatin (also known as GDF-8), a member of the TGFβ superfamily, is a negative regulator of muscle mass. Genetic loss of myostatin results in significantly increased muscle mass in multiple species including one case reported in human [55–58]. In preclinical models, pharmacologic inhibition of myostatin increases muscle mass and prevents muscle atrophy [59–63].