ArticleAmerican journal of physiology. Heart and circulatory physiology2008
In vivo administration of calpeptin attenuates calpain activation and cardiomyocyte loss in pressure-overloaded feline myocardium.
Article in American journal of physiology. Heart and circulatory physiology, 2008. 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, 50 citations in OpenAlex.
- Exercise triggers CAPN1-mediated AIF truncation, inducing myocyte cell death in arrhythmogenic cardiomyopathy.Science translational medicine · 2021Article
- Boceprevir, GC-376, and calpain inhibitors II, XII inhibit SARS-CoV-2 viral replication by targeting the viral main protease.Cell research · 2020Article
- Nuclear localization of a novel calpain-2 mediated junctophilin-2 C-terminal cleavage peptide promotes cardiomyocyte remodeling.Basic research in cardiology · 2020Article
- Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse.International journal of molecular sciences · 2020Review
- Pathophysiology of Acute and Chronic Right Heart Failure.Cardiology clinics · 2020Review
- Boceprevir, GC-376, and calpain inhibitors II, XII inhibit SARS-CoV-2 viral replication by targeting the viral main protease.bioRxiv : the preprint server for biology · 2020Article
- MiR-21 protected against diabetic cardiomyopathy induced diastolic dysfunction by targeting gelsolin.Cardiovascular diabetology · 2018Article
- Metabolic stress-induced cardiomyopathy is caused by mitochondrial dysfunction due to attenuated Erk5 signaling.Nature communications · 2017Article
- Structural and electrophysiological dysfunctions due to increased endoplasmic reticulum stress in a long-term pacing model using human induced pluripotent stem cell-derived ventricular cardiomyocytes.Stem cell research & therapy · 2017Article
- Differential role of calpain-dependent protein cleavage in intermediate and long-term operant memory in Aplysia.Neurobiology of learning and memory · 2017Article
- Proteases in cardiometabolic diseases: Pathophysiology, molecular mechanisms and clinical applications.Biochimica et biophysica acta · 2015Review
- Dasatinib Attenuates Pressure Overload Induced Cardiac Fibrosis in a Murine Transverse Aortic Constriction Model.PloS one · 2015Article
- Gelsolin (GSN) induces cardiomyocyte hypertrophy and BNP expression via p38 signaling and GATA-4 transcriptional factor activation.Molecular and cellular biochemistry · 2014Article
- Identification of the immunoproteasome as a novel regulator of skeletal muscle differentiation.Molecular and cellular biology · 2014Article
- Article
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
- Article
- Time course of right ventricular pressure-overload induced myocardial fibrosis: relationship to changes in fibroblast postsynthetic procollagen processing.American journal of physiology. Heart and circulatory physiology · 2012Article
- Regulation and physiological roles of the calpain system in muscular disorders.Cardiovascular research · 2012Review
- Calpain inhibition preserves talin and attenuates right heart failure in acute pulmonary hypertension.American journal of respiratory cell and molecular biology · 2012Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Calpain activation is linked to the cleavage of several cytoskeletal proteins and could be an important contributor to the loss of cardiomyocytes and contractile dysfunction during cardiac pressure overload (PO). Using a feline right ventricular (RV) PO model, we analyzed calpain activation during the early compensatory period of cardiac hypertrophy. Calpain enrichment and its increased activity with a reduced calpastatin level were observed in 24- to 48-h-PO myocardium, and these changes returned to basal level by 1 wk of PO. Histochemical studies in 24-h-PO myocardium revealed the presence of TdT-mediated dUTP nick-end label (TUNEL)-positive cardiomyocytes, which exhibited enrichment of calpain and gelsolin. Biochemical studies showed an increase in histone H2B phosphorylation and cytoskeletal binding and cleavage of gelsolin, which indicate programmed cardiomyocyte cell death. To test whether calpain inhibition could prevent these changes, we administered calpeptin (0.6 mg/kg iv) by bolus injections twice, 15 min before and 6 h after induction of 24-h PO. Calpeptin blocked the following PO-induced changes: calpain enrichment and activation, decreased calpastatin level, caspase-3 activation, enrichment and cleavage of gelsolin, TUNEL staining, and histone H2B phosphorylation. Although similar administration of a caspase inhibitor, N-benzoylcarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VD-fmk), blocked caspase-3 activation, it did not alleviate other aforementioned changes. These results indicate that biochemical markers of cardiomyocyte cell death, such as sarcomeric disarray, gelsolin cleavage, and TUNEL-positive nuclei, are mediated, at least in part, by calpain and that calpeptin may serve as a potential therapeutic agent to prevent cardiomyocyte loss and preserve myocardial structure and function during cardiac hypertrophy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.