ArticleActa pharmacologica Sinica2013
Pharmacological inhibition of myostatin/TGF-β receptor/pSmad3 signaling rescues muscle regenerative responses in mouse model of type 1 diabetes.
Article in Acta pharmacologica Sinica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Intrinsic muscle stem cell dysfunction underlies functional deficits in models of type 1 diabetes.NPJ Regenerative medicine · 2026Article
- Insights into intramuscular adipose-muscle signaling in the diabetic lower extremity.Journal of clinical & translational endocrinology · 2025Article
- The Effect of Geranylgeraniol and Ginger on Satellite Cells Myogenic State in Type 2 Diabetic Rats.Current issues in molecular biology · 2024Article
- Article
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Bioactive peptides laden nano and micro-sized particles enriched ECM inspired dressing for skin regeneration in diabetic wounds.Materials today. Bio · 2022Article
- Myostatin serum levels in children with type 1 diabetes mellitus.Hormones (Athens, Greece) · 2021Article
- Current Thoughts of Notch's Role in Myoblast Regulation and Muscle-Associated Disease.International journal of environmental research and public health · 2021Review
- Statins induce skeletal muscle atrophy via GGPP depletion-dependent myostatin overexpression in skeletal muscle and brown adipose tissue.Cell biology and toxicology · 2021Article
- Myogenetic Oligodeoxynucleotide (myoDN) Recovers the Differentiation of Skeletal Muscle Myoblasts Deteriorated by Diabetes Mellitus.Frontiers in physiology · 2021Article
- Mitochondrial Function in Muscle Stem Cell Fates.Frontiers in cell and developmental biology · 2020Review
- Improvement of Skeletal Muscle Regeneration by Platelet-Rich Plasma in Rats with Experimental Chronic Hyperglycemia.BioMed research international · 2020Article
- Diabetes-Induced Dysfunction of Mitochondria and Stem Cells in Skeletal Muscle and the Nervous System.International journal of molecular sciences · 2017Review
- Preventing aging with stem cell rejuvenation: Feasible or infeasible?World journal of stem cells · 2017Article
- Treadmill running induces satellite cell activation in diabetic mice.Biochemistry and biophysics reports · 2016Article
- Myostatin inhibition therapy for insulin-deficient type 1 diabetes.Scientific reports · 2016Article
- Skeletal muscle as a therapeutic target for delaying type 1 diabetic complications.World journal of diabetes · 2015Review
- Review
- Genetic disruption of Smad7 impairs skeletal muscle growth and regeneration.The Journal of physiology · 2015Article
- Systemic attenuation of the TGF-β pathway by a single drug simultaneously rejuvenates hippocampal neurogenesis and myogenesis in the same old mammal.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
aimTo study the influence of acute experimental diabetes on the regenerative potential of muscle stem (satellite) cells in mice.
methodsMale C57BL/6 young mice were injected with a single dose of streptozotocin (STZ, 180 mg/kg, ip) to induce diabetes. The diabetic mice were treated with insulin (0.75 U/kg, ip), follistatin (12 μg/kg, im) or Alk5 inhibitor (5 μmol/L per kg, sc) once a day. On the first day when high glucose levels were found, cardiotoxin (CTX) was focally injected into tibialis anterior and gastronemius muscles of the mice. The muscles were harvested 3 d and 5 d after CTX injection, and myofibers and satellite cells were isolated. Quantitative ex-vivo and in-vivo assays of myogenic potential were used to evaluate the muscle regenerative responses.
resultsThe satellite cells from the diabetic mice 3 d after CTX injection fail to activate, and the repair of muscle deteriorates, resembling that observed in old control mice. Furthermore, the satellite cells have excessive levels of myostatin, TGF-β receptor 1, pSmad3 and the cell cycle inhibitor p15, while the level of TGF-β1 remain unchanged. Treatment of the diabetic mice with insulin rescued muscle regenerative responses, and restored the expression levels of myostatin, TGF-β receptor 1, pSmad3, and p15 to those similar of healthy controls. Treatment of the diabetic mice with the myostatin antagonist follistatin, or with the Alk5 inhibitor of TGF-β receptor 1 (which did not diminish the blood glucose levels) rescued muscle regenerative responses and attenuated the myostatin/TGFβ receptor/pSmad3 signaling.
conclusionThe muscle regenerative responses are incapacitated and repair of the tissue fails within hours after the initiation of hyperglycemia in a mouse model of type 1 diabetes, but stem cell function is rescued by insulin, as well as follistatin or an Alk5 inhibitor that blocks TGF-β receptor signaling.
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