ReviewCirculation research2011
Tear me down: role of calpain in the development of cardiac ventricular hypertrophy.
Review in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Calpain inhibition in a transgenic model of calpastatin overexpression facilitates reversal of myocardial hypertrophy.ESC heart failure · 2025Article
- 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
- Therapeutic potential ofFrontiers in nutrition · 2025Review
- Novel Genetic Variants Associated with Primary Myocardial Fibrosis in Sudden Cardiac Death Victims.Journal of cardiovascular translational research · 2024Article
- Efficacy of a cysteine protease inhibitor compared with enalapril in murine heart failure models.iScience · 2024Article
- Proteolytic degradation of atrial sarcomere proteins underlies contractile defects in atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2024Article
- Calpain inhibition takes center stage against atrial fibrillation in the diabetic heart.Heart rhythm · 2024Article
- Rare variants inHGG advances · 2023Article
- Calpain-Mediated Mitochondrial Damage: An Emerging Mechanism Contributing to Cardiac Disease.Cells · 2021Review
- Protective effects of cardiac resynchronization therapy in a canine model with experimental heart failure by improving mitochondrial function: a mitochondrial proteomics study.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2021Article
- Creating a 'Molecular Band-Aid'; Blocking an Exposed Protease Target Site in Desmoplakin.Journal of personalized medicine · 2021Article
- SERCA2a ameliorates cardiomyocyte T-tubule remodeling via the calpain/JPH2 pathway to improve cardiac function in myocardial ischemia/reperfusion mice.Scientific reports · 2021Article
- The βFrontiers in cardiovascular medicine · 2021Article
- Nuclear localization of a novel calpain-2 mediated junctophilin-2 C-terminal cleavage peptide promotes cardiomyocyte remodeling.Basic research in cardiology · 2020Article
- Can We Prevent Mitochondrial Dysfunction and Diabetic Cardiomyopathy in Type 1 Diabetes Mellitus? Pathophysiology and Treatment Options.International journal of molecular sciences · 2020Review
- Ablation of the calpain-targeted site in cardiac myosin binding protein-C is cardioprotective during ischemia-reperfusion injury.Journal of molecular and cellular cardiology · 2019Article
- TFAM overexpression reduces pathological cardiac remodeling.Molecular and cellular biochemistry · 2019Article
- Article
- E-C coupling structural protein junctophilin-2 encodes a stress-adaptive transcription regulator.Science (New York, N.Y.) · 2018Article
- Over-expression of calpastatin attenuates myocardial injury following myocardial infarction by inhibiting endoplasmic reticulum stress.Journal of thoracic disease · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac hypertrophy develops most commonly in response to hypertension and is an independent risk factor for the development of heart failure. The mechanisms by which cardiac hypertrophy may be reversed to reduce this risk have not been fully determined to the point where mechanism-specific therapies have been developed. Recently, proteases in the calpain family have been implicated in the regulation of the development of cardiac hypertrophy in preclinical animal models. In this review, we summarize the molecular mechanisms by which calpain inhibition has been shown to modulate the development of cardiac (specifically ventricular) hypertrophy. The context within which calpain inhibition might be developed for therapeutic intervention of cardiac hypertrophy is then discussed.
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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.