Myostatin: a potential therapeutic target for metabolic syndrome
Open accessAbstract
Metabolic syndrome is a complex metabolic disorder, its main clinical manifestations are obesity, hyperglycemia, hypertension and hyperlipidemia. Although metabolic syndrome has been the focus of research in recent decades, it has been proposed that the occurrence and development of metabolic syndrome is related to pathophysiological processes such as insulin resistance, adipose tissue dysfunction and chronic inflammation, but there is still a lack of favorable clinical prevention and treatment measures for metabolic syndrome. Multiple studies have shown that myostatin (MSTN), a member of the TGF-β family, is involved in the development and development of obesity, hyperlipidemia, diabetes, and hypertension (clinical manifestations of metabolic syndrome), and thus may be a potential therapeutic target for metabolic syndrome. In this review, we describe the transcriptional regulation and receptor binding pathway of MSTN, then introduce the role of MSTN in regulating mitochondrial function and autophagy, review the research progress of MSTN in metabolic syndrome. Finally summarize some MSTN inhibitors under clinical trial and proposed the use of MSTN inhibitor as a potential target for the treatment of metabolic syndrome.
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MSTN activates TGF-β signaling, inhibits endothelial nitric oxide synthase phosphorylation, reduces NO production, and leads to impaired vasodilation.
“For example, by activating TGF-β signaling, MSTN inhibits endothelial nitric oxide synthase (eNOS) phosphorylation, reducing NO production and leading to impaired vasodilation; it also upregulates vascular cell adhesion molecule-1 (VCAM-1) expression, promoting monocyte adhesion to the endothelium and initiating vascular wall inflammation [60].”
From Exercise-Induced Myokines in Obesity-Related Metabolic Disorders and Cardiovascular Protection: A Narrative Review (2026) · cites this paper as [60]
The ‘Brief review of MSTN’ section identifies MSTN as a TGF-β-family member and describes its receptor-mediated Smad2/3 signaling. It does not support the attributed mechanism involving reduced eNOS phosphorylation, NO production, or vasodilation; searches for eNOS, nitric oxide, and VCAM-1 also found no support for the sentence’s vascular claims. The ‘MSTN in hypertension’ section discusses associations with blood pressure but says the mechanisms remain to be uncovered. (LLM, conf=0.85)
Experimental — accuracy not yet measuredMSTN upregulates MCP-1, forming a positive feedback loop of inflammation that accelerates inflammatory cell infiltration and lipid deposition.
“Additionally, MSTN upregulates monocyte chemoattractant protein-1 (MCP-1), forming a positive feedback loop of inflammation that accelerates inflammatory cell infiltration and lipid deposition [60].”
From Exercise-Induced Myokines in Obesity-Related Metabolic Disorders and Cardiovascular Protection: A Narrative Review (2026) · cites this paper as [60]
The ‘MSTN in obesity and hyperlipemia’ section reports that MSTN deficiency reduces lipid accumulation in mice. It does not describe MSTN upregulating MCP-1, an inflammatory feedback loop, or inflammatory-cell infiltration; searches for MCP-1 and those mechanisms found no supporting passage. Page numbers were not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredClinical trials of MSTN inhibitors for sarcopenia and muscular dystrophies are ongoing, though their cardiovascular effects warrant careful evaluation given MSTN's direct pro-atherogenic actions.
“Clinical trials of MSTN inhibitors for sarcopenia and muscular dystrophies are ongoing, though their cardiovascular effects warrant careful evaluation given MSTN’s direct pro-atherogenic actions [60].”
From Exercise-Induced Myokines in Obesity-Related Metabolic Disorders and Cardiovascular Protection: A Narrative Review (2026) · cites this paper as [60]
The inhibitor of MSTN section says inhibitors have been developed for patients with sarcopenia and muscular dystrophy and that some compounds are being tested in clinical trials. It does not describe direct pro-atherogenic actions of MSTN or call for cardiovascular evaluation of these trials. The Autophagy section instead reports that MSTN deficiency aggravated a cardiac condition in mice, which is not evidence of pro-atherogenic action. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMSTN upregulates VCAM-1, promoting monocyte adhesion to the endothelium and initiating vascular wall inflammation.
“For example, by activating TGF-β signaling, MSTN inhibits endothelial nitric oxide synthase (eNOS) phosphorylation, reducing NO production and leading to impaired vasodilation; it also upregulates vascular cell adhesion molecule-1 (VCAM-1) expression, promoting monocyte adhesion to the endothelium and initiating vascular wall inflammation [60].”
From Exercise-Induced Myokines in Obesity-Related Metabolic Disorders and Cardiovascular Protection: A Narrative Review (2026) · cites this paper as [60]
The ‘MSTN in hypertension’ section reports an association with blood pressure but says the mechanisms remain to be uncovered. Searches of our copy for VCAM-1, monocyte adhesion, and endothelial inflammation found no passage describing the claimed pathway. No page number is available in our copy. (LLM, conf=0.75)
Experimental — accuracy not yet measured
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Myostatin deficiency is associated with lipidomic abnormalities in skeletal muscles
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Mss51 deletion enhances muscle metabolism and glucose homeostasis in mice
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Zhang, Y., & Qiu, Y. (2026) · Sports · doi:10.3390/sports14050212 · Cited by 3 · see citing works
“Additionally, MSTN upregulates monocyte chemoattractant protein-1 (MCP-1), forming a positive feedback loop of inflammation that accelerates inflammatory cell infiltration and lipid deposition [60].”
Influential
- Authors
- Yang, M., Liu, C., Jiang, N., Liu, Y., Luo, S., Li, C., Zhao, H., Han, Y., Chen, W., Li, L., Xiao, L., & Sun, L.
- Affiliations
- Second Xiangya Hospital of Central South University (CN)
- Corresponding author
- Sun, Lin
- Venue
- Frontiers in Endocrinology
- Publisher
- Frontiers Media SA
- Published
- 2023-05-23
- Volume
- 14
- Pages
- 1181913-1181913
- ISSN
- 1664-2392 (ISSN-L)
- PMC
- PMC10242177
- OpenAlex
- W4378085175
- Cited by
- 33
- References
- 106
- Citations by year
- 2026: 10 · 2025: 16 · 2024: 6 · 2023: 1
- FWCI
- 1.29
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Endocrinology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Natural Science Foundation of Hunan Province (2021JC0003)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- myostatin, metabolic syndrome, obesity, hyperlipidemia, hypertension, insulin resistance, adipose tissue dysfunction, chronic inflammation, TGF-beta superfamily, mitochondrial function, autophagy, therapeutic target
- MeSH terms
- Humans, Insulin Resistance, Obesity, Muscle, Skeletal, Metabolic Syndrome, Myostatin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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