Follistatin-344: Research in Muscle Cell Regeneration

by | Mar 1, 2022 | Research

Follistatin-344 has been linked to an interplay with the naturally occurring biopeptide Myostatin. Myostatin is a peptide that is released by muscle cells, also known as myocytes, and belongs to the Transforming Growth Factor-Beta (TGF-β) family. Myostatin appears have the ability to inhibit the growth and differentiation of muscle cells, and there are suggestions that it could lead to muscle fibrosis and shrinkage of organs such as the heart.

Research and isolation of Follistatin, a protein that is naturally produced, has led researchers to develop a synthetic version called Follistatin-344. The primary speculation is that Follistatin-344 peptide antagonizes the function of TGF-β. The TGF-β family comprises Follicle Stimulating Hormone (FSH), Myostatin, and Activin. In addition to potentially inhibiting TGF-β, Follistatin-344 might act on the IGF-1/Insulin pathway.

 

Follistatin-344 Peptide Research

Follistatin-344 peptide has been employed in research studies with a variety of focuses, though it is primarily examined within the context of muscle cells.

1. Muscle Cell Growth: As mentioned, myostatin functions to reduce muscle mass, and is a member of the TGF-1 family that inhibits the growth and differentiation of muscle fibers. There are suggestions that Follistatin-344 peptide may exert potent anti-myostatin action. Speculative research on mice lacking myostatin indicates that the peptide may induce greater muscle mass development. Additionally, speculative studies on Follistatin-344 peptide have suggested a remarkable increase in muscle mass without the involvement of other muscle-building factors. Follistatin-344 has been suggested to increase muscle bulk through two main mechanisms: hypertrophy and hyperplasia. Hypertrophy leads to an increase in the size of individual muscle cells, while hyperplasia increases the number of muscle fibers.

2. Speculative Effects on Diabetes Mellitus Type 1 diabetes, considered to result from a reduced expression of insulin-secreting beta-pancreatic cells, leads to reduced insulin secretion and poor glucose metabolism. Follistatin-344 peptide, following studies in animal research models, appears to lead to an increase in beta-pancreatic cells. The exposure of Follistatin-344 peptide in animal models resulted in a remarkable rise in the life expectancy of mice and a reduction in diabetes-related micro- or macro-vascular complications.

3. Follistatin-344 peptide and Breast Cancer Speculative research on the effects and levels of Follistatin in female research models of breast cancer  involved Reverse Transcription Polymerase Chain Reaction (RT-PCR) to check natural peptide levels. Results taken from females with under-expressed Follistatin indicated that only a few had normal or higher levels of Follistatin. Higher levels of Follistatin could be associated with a lower incidence of disease metastasis and a better prognosis.

4. Speculative Effects on Esophageal and Liver Cancer Barrett’s esophagus, a premalignant condition, involves transforming cells in the lower esophagus. Bone Morphogenetic Protein (BMP) might be a primary factor behind the metaplasia of the esophagus. Speculative research suggests that Follistatin may counteract the action of BMP and potentially prevent the development of esophageal cancer. Additionally, liver fibrosis, a condition predisposing to hepatocellular carcinoma, might see a significant improvement in the lifespan of liver cells (hepatocytes) with Follistatin. The peptide was suggested to reduce the risk of liver fibrosis by 32%, potentially leading to a reduction in the risk of hepatocellular carcinoma.

 

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Dr. Usman

Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.