FOLLISTATIN 344
Follistatin 344 Protein Description
Follistatin-344 (FS344) is a synthetic version of the naturally occurring protein follistatin, which is part of the TGF-β (transforming growth factor-beta) family. This protein plays a critical role in regulating muscle growth and other physiological processes by inhibiting myostatin, activin, and follicle-stimulating hormone (FSH). FS344 is specifically engineered for research purposes, particularly in the context of muscle enhancement and regenerative medicine.
Follistatin 344 Structure
Molecular Weight: 3780 g/mol
PubChem CID: 178101631
Synonyms:
Activin-Binding Protein
FSH-Suppressing Protein
FST
FS-344
Research Areas:
Muscle Disorders
Muscle Hypertrophy
Chronic Kidney Disease (CKD)
Vascular Function
Breast Cancer Research
Follistatin 344 Research
Follistatin 344 (FS344) is a variant of the follistatin protein, which is known for its role in inhibiting myostatin, a protein that negatively regulates muscle growth. This makes FS344 a subject of interest in both therapeutic applications and performance enhancement research contexts. FS344 is one of the two main isoforms of follistatin, the other being FS317, both of which arise from alternative splicing of the follistatin precursor mRNA.
Follistatin and Muscle Disorders
FS344 has shown promise in gene therapy for muscle disorders such as Becker muscular dystrophy. Its ability to increase muscle mass by inhibiting the myostatin pathway has been demonstrated in preclinical studies, and clinical trials are exploring its potential as a genetic enhancer to improve muscle function.1
Follistatin and Muscle Hypertrophy
Follistatin (FS) is a potent inhibitor of myostatin, a negative regulator of muscle growth, and has been shown to induce significant muscle hypertrophy. The hypertrophic effects of FS are mediated through multiple pathways, including the inhibition of myostatin and activin, both members of the TGF-beta superfamily. FS overexpression leads to increased muscle mass by promoting satellite cell proliferation and inhibiting these growth inhibitors.2
FS-induced muscle hypertrophy also has beneficial effects on neuromuscular function, particularly in aged mice. Overexpression of FS improves neuromuscular junction innervation and function, countering age-related degeneration, although it does not prevent motor unit loss.3
Follistatin in Chronic Kidney Disease (CKD)
The therapeutic potential of follistatin in CKD is highlighted by its ability to ameliorate fibrosis and improve kidney function in experimental models4. Follistatin administration has been shown to protect against diabetic kidney disease by attenuating early disease markers such as albuminuria and glomerular matrix accumulation5. Additionally, inhibition of miR299a-5p, which suppresses the antifibrotic actions of follistatin, offers a novel therapeutic approach for CKD by protecting against renal fibrosis6.
Effects on Vascular Function
Studies using spontaneously hypertensive rats (SHR) have demonstrated that follistatin treatment lowers BP and enhances vascular health. This is achieved through the reduction of vascular ROS, improvement in endothelium-dependent relaxation, and inhibition of hypercontractility. Follistatin also reduces the size of adipocytes and increases the expression of brown adipose tissue markers, indicating a shift from white to brown PVAT, which is beneficial for vascular function.7
Follistatin as a Metastasis Suppressor
Research indicates that follistatin may act as a metastasis suppressor in breast cancer. In a mouse model of HER2-positive breast cancer, overexpression of follistatin was shown to block the formation of lung metastases, although it did not affect primary tumor growth8. This suggests that follistatin could be a target for therapeutic strategies aimed at preventing metastatic progression in breast cancer.
References
Al-Zaidy, S., Sahenk, Z., Rodino-Klapac, L., Kaspar, B., & Mendell, J. (2015). Follistatin Gene Therapy Improves Ambulation in Becker Muscular Dystrophy. Journal of Neuromuscular Diseases, 2, 185 – 192. https://doi.org/10.3233/JND-150083.
Gilson, H., Schakman, O., Kalista, S., Lause, P., Tsuchida, K., & Thissen, J. (2009). Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin.. American journal of physiology. Endocrinology and metabolism, 297 1, E157-64 . https://doi.org/10.1152/ajpendo.00193.2009.
Iyer, C., Chugh, D., Bobbili, P., J., A., Crum, A., Yi, A., Kaspar, B., Meyer, K., Burghes, A., & Arnold, W. (2021). Follistatin-induced muscle hypertrophy in aged mice improves neuromuscular junction innervation and function. Neurobiology of Aging, 104, 32-41. https://doi.org/10.1016/j.neurobiolaging.2021.03.005.
Mehta, N., Gava, Á., Zhang, D., Gao, B., & Krepinsky, J. (2019). Follistatin Protects against Glomerular Mesangial Cell Apoptosis and Oxidative Stress to Ameliorate Chronic Kidney Disease.. Antioxidants & redox signaling. https://doi.org/10.1089/ars.2018.7684.
Zhang, D., Gava, Á., Van Krieken, R., Mehta, N., Li, R., Gao, B., Desjardins, E., Steinberg, G., Hawke, T., & Krepinsky, J. (2019). The caveolin-1 regulated protein follistatin protects against diabetic kidney disease.. Kidney international. https://doi.org/10.1016/J.KINT.2019.05.032.
Mehta, N., Li, R., Zhang, D., Soomro, A., He, J., Zhang, I., MacDonald, M., Gao, B., & Krepinsky, J. (2021). miR299a-5p promotes renal fibrosis by suppressing the antifibrotic actions of follistatin. Scientific Reports, 11. https://doi.org/10.1038/s41598-020-80199-z.
Kuganathan, A., Lu, V., Gao, B., Macdonald, M., Dickhout, J., & Krepinsky, J. (2024). Abstract P448: Follistatin Improves Vascular Function by Regulating Perivascular Adipose Tissue in Essential Hypertension. Hypertension. https://doi.org/10.1161/hyp.81.suppl_1.p448.
Seachrist, D., Sizemore, S., Johnson, E., Abdul-Karim, F., Bonk, K., & Keri, R. (2017). Follistatin is a metastasis suppressor in a mouse model of HER2-positive breast cancer. Breast Cancer Research, 19. https://doi.org/10.1186/s13058-017-0857-y.
Disclaimer: For Research Purposes Only
This content is provided strictly for research purposes and does not constitute an endorsement or recommendation for the non-laboratory application or improper handling of peptides designed for research. The information, including discussions about specific peptides and their researched benefits, is presented for informational purposes only and must not be construed as health, clinical, or legal guidance, nor an encouragement for non-research use in humans. Peptides described here are solely for use in structured scientific study by authorized individuals. We advise consulting with research experts, medical practitioners, or legal counsel prior to any decisions about obtaining or utilizing these peptides. The expectation of responsible, ethical utilization of this information for legitimate investigative and scholarly objectives is paramount. This notice is dynamic and governs all provided content on research peptides.