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Myositis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Follistatin is a gene therapy that leads to muscle growth. A small phase 1 study was performed on six patients and showed an improvement in a six-minute-walk test and a decrease in fibrosis on muscle biopsies.130 However, the study had significant limitations.131
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
Follistatin is a protein known to inhibit members of the TGFβ superfamily, including myostatin (2). By neutralizing circulating myostatin, FST can increase skeletal muscle mass (73, 74). Treating non-human primates with FST led to muscle hypertrophy (66). FST can also stimulate insulin and glucagon secretion from the pancreas (44).
Regulation of Reproduction by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The testes also produce several protein hormones that include activin, inhibin, and follistatin [26]. Inhibins are released into the blood and suppress pituitary FSH secretion, whereas activins mostly exert their actions as local paracrine/autocrine growth factors. Follistatin is a potent activin binding protein, which also modulates local biological functions. Inhibin is a dimeric glycoprotein existing in two bioactive forms: A and B. Inhibin B shows temporal changes in its expression with the changing role of the Sertoli cell in immature and adult testes. In the adult, the levels of inhibin B are positively correlated with sperm number and spermatogenic status and are negatively correlated with serum FSH levels. Production of inhibin B is regulated by complex interactions between FSH, Sertoli cells, Leydig cells, and germ cells. Inhibin may also play a role at autocrine or paracrine levels in modulating the actions of activin. Other compounds such as opioids, GnRH-like peptides, vasopressin, oxytocin, and several growth factors have also been detected in the testes and appear to function as paracrine agents.
The effects of gradual vs. rapid weight loss on serum concentrations of myokines and body composition in overweight and obese females
Published in Archives of Physiology and Biochemistry, 2023
Reza Bagheri, Damoon Ashtary-Larky, Bradley T Elliott, Darryn S. Willoughby, Mehdi Kargarfard, Meysam Alipour, Nasrin Lamuchi-Deli, Wesam Kooti, Omid Asbaghi, Alexei Wong
MST is a member of transforming growth factor-beta (TGF-β) family member which inhibits muscle differentiation and growth (Allen et al. 2011). Mice in which MST processing or signalling is disrupted exhibited muscle mass gains (Yang et al. 2001, Matsakas et al. 2009), while MST over-expression resulted in a significant decrements of muscle mass (Reisz-Porszasz et al. 2003). These results confirm MST’s critical role in inhibiting muscle mass gains. Follistatin is a member of the TGF-β superfamily (Görgens et al. 2013), which is ubiquitously expressed in all tissues of the human body, including skeletal muscle, and has both paracrine and autocrine influences. FST has shown to bind MST and inhibit its activity (Nakatani et al. 2011), but also can bind and inhibit other TGF-β family members (Tsuchida et al. 2000), suggesting a more diverse physiological role. Obesity is associated with increased MST expression in both adipose and skeletal muscle tissues (Allen et al. 2011), and MST mRNA levels decreased during weight loss following daily injection of recombinant leptin in mice (Allen et al. 2008). Similarly, circulating FST concentration is also elevated in obese individuals relative to normal weight controls (Maïmoun et al. 2020), concentration of which is subsequently reduced following bariatric surgery-induced weight loss (Wiewiora et al. 2020). These results highlight a role of weight loss to reduce MST and FST concentrations.
Inflammatory myopathies: shedding light on promising agents and combination therapies in clinical trials
Published in Expert Opinion on Investigational Drugs, 2021
Rachel Zeng, Stefanie Glaubitz, Jens Schmidt
Follistatin antagonizes the effects of myostatin and thereby promotes skeletal muscle growth. As this bears the potential to treat muscle atrophy, a novel gene therapy with AAV vectors encoding a follistatin isoform was tested in a small open-label study with six male IBM patients [95]. The treatment was injected in the quadriceps muscles of both legs. Improvement in the 6MWD was the primary outcome. Additionally, all patients had an exercise regime three times a week. After one year of the injection-treated patients showed mild improvement in the 6MWT compared to untreated patients, who were matched for gender and age, but these results need to interpreted very carefully in view of this very low number of patients. The posttreatment muscle biopsy showed reduced fibrosis and increased muscle regeneration.
The lncRNA PVT1/miR-590-5p/FSTL1 axis modulates the proliferation and migration of airway smooth muscle cells in asthma
Published in Autoimmunity, 2021
Wen-Lan Wang, Xiao-Ming Luo, Qin Zhang, Hai-Qiao Zhu, Guo-Qing Chen, Qin Zhou
Accumulating evidence shows the effects of miRNAs on ASMCs by gene regulation. For example, similarly, adenovirus-mediated overexpression of miR-638 has been observed to significantly suppress proliferation and migration of ASMCs through target-inhibition on cyclin D1 and NOR1 [31]. Of note, relation analysis between miRNAs and their target genes has been highlighted to be of importance to childhood asthma phenotypes [32]. A functional study has elaborated miR-590-5p curbs proliferative potential of foetal ASMCs by downregulating STAT3 [21]. Correspondingly, downstream regulatory mechanism of miR-590-5p in ASMCs was studied in our study, revealing FSTL1 as a target gene of miR-590-5p. FSTL1, a member of the follistatin protein family, has a characteristic structure unit found in follistatin, called the FS domain and modulates the formation of organ tissue in embryos [33]. Knockdown of FSTL1 has been documented as a promising therapeutic target for childhood asthma with regard to airway remodelling by causing the inhibition on ASMCs proliferation and migration after exposure to PDGF-BB [22,34]. Additionally, FSTL1 has been suggested to also be functional for epithelial-mesenchymal transition and airway remodelling in patients suffering from refractory asthma [35]. In our study, we found that overexpressed FSTL1 could enhance proliferative and migrative capabilities of ASMCs triggered by PDGF-BB while counterweighing the action of miR-590-5p mimic.