MOTS-c Peptide Attenuated Diabetic Cardiomyopathy in STZ-Induced Type 1 Diabetic Mouse Model
Author:
Publisher
Springer Science and Business Media LLC
Subject
Pharmacology (medical),Cardiology and Cardiovascular Medicine,Pharmacology,General Medicine
Link
https://link.springer.com/content/pdf/10.1007/s10557-023-07540-2.pdf
Reference26 articles.
1. Li Y, Ma J, Zhu H, et al. Targeted inhibition of calpain reduces myocardial hypertrophy and fibrosis in mouse models of type 1 diabetes. Diabetes. 2011;60(11):2985–94. https://doi.org/10.2337/db10-1333.
2. Xie Z, Lau K, Eby B, et al. Improvement of cardiac functions by chronic metformin treatment is associated with enhanced cardiac autophagy in diabetic OVE26 mice. Diabetes. 2011;60(6):1770–8. https://doi.org/10.2337/db10-0351.
3. Wu S, Lu Q, Ding Y, et al. Hyperglycemia-driven inhibition of AMP-activated protein kinase α2 induces diabetic cardiomyopathy by promoting mitochondria-associated endoplasmic reticulum membranes in vivo. Circulation. 2019;139(16):1913–36. https://doi.org/10.1161/circulationaha.118.033552.
4. Yuan J, Wang M, Pan Y, et al. The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats. Sci Rep. 2021;11(1):20077. https://doi.org/10.1038/s41598-021-99568-3.
5. Zhong P, Peng J, Liu T, Ding HS. AAV9-mediated cardiac CNTF overexpression exacerbated adverse cardiac remodeling in streptozotocin-induced type 1 diabetic models. Cardiovasc Toxicol. 2022;22(1):88–96. https://doi.org/10.1007/s12012-021-09706-6.
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