ArticlePloS one2015
Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Efficacy of a cysteine protease inhibitor compared with enalapril in murine heart failure models.iScience · 2024Article
- Calpain inhibition takes center stage against atrial fibrillation in the diabetic heart.Heart rhythm · 2024Article
- Calpain inhibition decreases oxidative stress via mitochondrial regulation in a swine model of chronic myocardial ischemia.Free radical biology & medicine · 2023Article
- Calpain: the regulatory point of myocardial ischemia-reperfusion injury.Frontiers in cardiovascular medicine · 2023Review
- Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022Review
- Spatio-temporal regulation of calpain activity after experimental myocardial infarction in vivo.Biochemistry and biophysics reports · 2021Article
- Nuclear localization of a novel calpain-2 mediated junctophilin-2 C-terminal cleavage peptide promotes cardiomyocyte remodeling.Basic research in cardiology · 2020Article
- Inhibition of GPR35 Preserves Mitochondrial Function After Myocardial Infarction by Targeting Calpain 1/2.Journal of cardiovascular pharmacology · 2020Article
- p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Over-expression of calpastatin attenuates myocardial injury following myocardial infarction by inhibiting endoplasmic reticulum stress.Journal of thoracic disease · 2018Article
- Targeting Calpain for Heart Failure Therapy: Implications From Multiple Murine Models.JACC. Basic to translational science · 2018Article
- Unexpected role of the L-domain of calpastatin during the autoproteolytic activation of human erythrocyte calpain.Bioscience reports · 2018Article
- Article
- The inhibition of calpains ameliorates vascular restenosis through MMP2/TGF-β1 pathway.Scientific reports · 2016Article
- Expression of calcineurin, calpastatin and heat shock proteins during ischemia and reperfusion.Biochemistry and biophysics reports · 2015Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCalpain is activated following myocardial infarction and ablation of calpastatin (CAST), an endogenous inhibitor of calpains, promotes left ventricular remodeling after myocardial infarction (MI). The present study aimed to investigate the effect of transgenic over-expression of CAST on the post-infarction myocardial remodeling process.
methodWe established transgenic mice (TG) ubiquitously over-expressing human CAST protein and produced MI in TG mice and C57BL/6J wild-type (WT) littermates.
resultsThe CAST protein expression was profoundly upregulated in the myocardial tissue of TG mice compared with WT littermates (P < 0.01). Overexpression of CAST significantly reduced the infarct size (P < 0.01) and blunted MI-induced interventricular hypertrophy, global myocardial fibrosis and collagen I and collagen III deposition, hypotension and hemodynamic disturbances at 21 days after MI. Moreover, the MI-induced up-regulation and activation of calpains were obviously attenuated in CAST TG mice. MI-induced down-regulation of CAST was partially reversed in TG mice. Additionally, the MI-caused imbalance of matrix metalloproteinases and their inhibitors was improved in TG mice.
conclusionsTransgenic over-expression of CAST inhibits calpain activation and attenuates post-infarction myocardial remodeling.
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