ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Calpain inhibition preserves myocardial structure and function following myocardial infarction.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Post-infarction KLHL40-mediated regulation of cardiac sarcomeric integrity and function.PeerJ · 2026Article
- The key role of Calpain in COVID-19 as a therapeutic strategy.Inflammopharmacology · 2022Review
- Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress.Antioxidants (Basel, Switzerland) · 2022Article
- Calpain Inhibitor Calpeptin Alleviates Ischemia/Reperfusion-Induced Acute Kidney InjuryFrontiers in medicine · 2022Article
- Targeted inhibition of calpain in mitochondria alleviates oxidative stress-induced myocardial injury.Acta pharmacologica Sinica · 2021Article
- Exercise triggers CAPN1-mediated AIF truncation, inducing myocyte cell death in arrhythmogenic cardiomyopathy.Science translational medicine · 2021Article
- Primary cilia defects causing mitral valve prolapse.Science translational medicine · 2019Article
- Over-expression of calpastatin attenuates myocardial injury following myocardial infarction by inhibiting endoplasmic reticulum stress.Journal of thoracic disease · 2018Article
- Pediatric Eosinophilic Esophagitis Endotypes: Are We Closer to Predicting Treatment Response?Clinical reviews in allergy & immunology · 2018Review
- CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain.EMBO molecular medicine · 2018Article
- Article
- Calpain-1 induces endoplasmic reticulum stress in promoting cardiomyocyte apoptosis following hypoxia/reoxygenation.Biochimica et biophysica acta · 2015Article
- Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling.PloS one · 2015Article
- Calpain system and its involvement in myocardial ischemia and reperfusion injury.World journal of cardiology · 2014Review
- Calpain-dependent cleavage of N-cadherin is involved in the progression of post-myocardial infarction remodeling.The Journal of biological chemistry · 2014Article
- Proteolysis of the human DNA polymerase delta smallest subunit p12 by μ-calpain in calcium-triggered apoptotic HeLa cells.PloS one · 2014Article
- Deficiency of Capn4 gene inhibits nuclear factor-κB (NF-κB) protein signaling/inflammation and reduces remodeling after myocardial infarction.The Journal of biological chemistry · 2012Article
- Article
- Targeted inhibition of calpain reduces myocardial hypertrophy and fibrosis in mouse models of type 1 diabetes.Diabetes · 2011Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca(2+)-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intravenously administered at 0.5 mg/kg body wt before MI induction and then at the same dose subcutaneously once per day. Both calpeptin-treated (n = 6) and untreated (n = 6) MI mice were used to study changes in myocardial structure and function after 4 days of MI, where end-diastolic volume (EDV) and left ventricular ejection fraction (EF) were measured by echocardiography. Calpain activation and programmed cell death were measured by immunohistochemistry, Western blotting, and TdT-mediated dUTP nick-end labeling (TUNEL). In MI mice, calpeptin treatment resulted in a significant improvement in EF [EF decreased from 67 + or - 2% pre-MI to 30 + or - 4% with MI only vs. 41 + or - 2% with MI + calpeptin] and attenuated the increase in EDV [EDV increased from 42 + or - 2 microl pre-MI to 73 + or - 4 microl with MI only vs. 55 + or - 4 microl with MI + calpeptin]. Furthermore, calpeptin treatment resulted in marked reduction in calpain- and caspase-3-associated changes and TUNEL staining. These studies indicate that calpain contributes to MI-induced alterations in myocardial structure and function and that it could be a potential therapeutic target in treating MI patients.
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Registered trials
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