ArticleThe Journal of biological chemistry2011
Calpain protects the heart from hemodynamic stress.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- The identification of adenylyl cyclase modulators as potential receptors for 6-nitrodopamine in human-induced pluripotent stem cell (hiPSC)-derived cardiomyocytes and their relevance in heart inotropism.Frontiers in pharmacology · 2025Article
- Article
- Targeting calpain-2-mediated junctophilin-2 cleavage delays heart failure progression following myocardial infarction.Journal of molecular and cellular cardiology · 2024Article
- Calpain: the regulatory point of myocardial ischemia-reperfusion injury.Frontiers in cardiovascular medicine · 2023Review
- Calpain-mediated proteolytic production of free amino acids in vascular endothelial cells augments obesity-induced hepatic steatosis.The Journal of biological chemistry · 2022Article
- Spatio-temporal regulation of calpain activity after experimental myocardial infarction in vivo.Biochemistry and biophysics reports · 2021Article
- Desmosomes: emerging pathways and non-canonical functions in cardiac arrhythmias and disease.Biophysical reviews · 2021Review
- Calpain-Mediated Mitochondrial Damage: An Emerging Mechanism Contributing to Cardiac Disease.Cells · 2021Review
- Review
- Plasma membrane integrity: implications for health and disease.BMC biology · 2021Review
- Mitochondrial dysfunction and consequences in calpain-3-deficient muscle.Skeletal muscle · 2020Article
- CAPN6 in disease: An emerging therapeutic target (Review).International journal of molecular medicine · 2020Review
- Implications of the complex biology and micro-environment of cardiac sarcomeres in the use of high affinity troponin antibodies as serum biomarkers for cardiac disorders.Journal of molecular and cellular cardiology · 2020Review
- Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse.International journal of molecular sciences · 2020Review
- Cardiomyocyte damage control in heart failure and the role of the sarcolemma.Journal of muscle research and cell motility · 2019Article
- Calpain-2 promotes MKP-1 expression protecting cardiomyocytes in both in vitro and in vivo mouse models of doxorubicin-induced cardiotoxicity.Archives of toxicology · 2019Article
- Sarcomeric protein modification during adrenergic stress enhances cross-bridge kinetics and cardiac output.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Calpain research for drug discovery: challenges and potential.Nature reviews. Drug discovery · 2016Review
- Resuscitation of a dead cardiomyocyte.Heart failure reviews · 2015Review
- Membrane Repair: Mechanisms and Pathophysiology.Physiological reviews · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calpains make up a family of Ca(2+)-dependent intracellular cysteine proteases that include ubiquitously expressed μ- and m-calpains. Both are heterodimers consisting of a distinct large catalytic subunit (calpain 1 for μ-calpain and calpain 2 for m-calpain) and a common regulatory subunit (calpain 4). The physiological roles of calpain remain unclear in the organs, including the heart, but it has been suggested that calpain is activated by Ca(2+) overload in diseased hearts, resulting in cardiac dysfunction. In this study, cardiac-specific calpain 4-deficient mice were generated to elucidate the role of calpain in the heart in response to hemodynamic stress. Cardiac-specific deletion of calpain 4 resulted in decreased protein levels of calpains 1 and 2 and showed no cardiac phenotypes under base-line conditions but caused left ventricle dilatation, contractile dysfunction, and heart failure with interstitial fibrosis 1 week after pressure overload. Pressure-overloaded calpain 4-deficient hearts took up a membrane-impermeant dye, Evans blue, indicating plasma membrane disruption. Membrane repair assays using a two-photon laser-scanning microscope revealed that calpain 4-deficient cardiomyocytes failed to reseal a plasma membrane that had been disrupted by laser irradiation. Thus, the data indicate that calpain protects the heart from hemodynamic stresses, such as pressure overload.
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Registered trials
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.