ArticleJournal of cardiovascular pharmacology2010
Lack of beta3 integrin signaling contributes to calpain-mediated myocardial cell loss in pressure-overloaded myocardium.
Article in Journal of cardiovascular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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
29 citing papers in PubMed, 41 citations in OpenAlex.
- Targeting Integrin β3 in Endothelial Cells Attenuates Cardiac Fibrosis Through the Calcium-Calmodulin-Dependent Protein Kinase IIα- cAMP-Responsive Element Binding Protein 1 Signaling Axis in Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2026Article
- CCDC141 is a Connectin/Titin and Nesprin-1 binding protein that adapts cardiomyocytes to mechanical stress.Communications biology · 2025Article
- β1 integrins regulate cellular behaviour and cardiomyocyte organization during ventricular wall formation.Cardiovascular research · 2024Article
- Epidermal Growth Factor-Like Repeats and Discoidin I-Like Domains 3 Deficiency Attenuates Dilated Cardiomyopathy by Inhibiting Ubiquitin Specific Peptidase 10 Dependent Smad4 Deubiquitination.Journal of the American Heart Association · 2024Article
- Rare variants inHGG advances · 2023Article
- Review on the protective mechanism of astragaloside IV against cardiovascular diseases.Frontiers in pharmacology · 2023Review
- Effect of cardioplegic arrest and reperfusion on left and right ventricular proteome/phosphoproteome in patients undergoing surgery for coronary or aortic valve disease.International journal of molecular medicine · 2022Article
- Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022Review
- Key Roles of RGD-Recognizing Integrins During Cardiac Development, on Cardiac Cells, and After Myocardial Infarction.Journal of cardiovascular translational research · 2022Review
- Integrins in cardiac hypertrophy: lessons learned from culture systems.ESC heart failure · 2021Review
- 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
- Integrin β3 promotes cardiomyocyte proliferation and attenuates hypoxia-induced apoptosis via regulating the PTEN/Akt/mTOR and ERK1/2 pathways.International journal of biological sciences · 2020Article
- Morphological and Functional Characteristics of Animal Models of Myocardial Fibrosis Induced by Pressure Overload.International journal of hypertension · 2020Review
- Extracorporeal shock waves protect cardiomyocytes from doxorubicin-induced cardiomyopathy by upregulating survivin via the integrin-ILK-Akt-Sp1/p53 axis.Scientific reports · 2019Article
- Suppression of angiotensin II-induced pathological changes in heart and kidney by the caveolin-1 scaffolding domain peptide.PloS one · 2018Article
- Integrins and integrin-related proteins in cardiac fibrosis.Journal of molecular and cellular cardiology · 2016Review
- 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
- Expressions of CD11a, CD11b, and CD11c integrin proteins in rats with myocardial hypertrophy.Iranian journal of basic medical sciences · 2014Article
- Nrf2 enhances myocardial clearance of toxic ubiquitinated proteins.Journal of molecular and cellular cardiology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Although cardiac hypertrophy initially ensues as a compensatory mechanism, it often culminates in congestive heart failure. Based on our earlier studies that calpain and beta3 integrin play cell death and survival roles, respectively, during pressure-overload (PO) hypertrophy, we investigated if the loss of beta3 integrin signaling is a potential mechanism for calpain-mediated cardiomyocyte death during PO. beta3 Integrin knockout (beta3) and wild-type mice were used to induce either moderate or severe PO in vivo for short-term (72-hour) and long-term (4-week) transverse aortic constriction. Whereas wild-type mice showed no changes during moderate PO at both time points, beta3 mice exhibited both enrichment of the mu-calpain isoform and programmed cell death of cardiomyocytes after 4-week PO. However, with severe PO that caused increased mortality in both mice groups, cell death was observed in wild-type mice also. To study calpain's role, calpeptin, a specific inhibitor of calpain, was administered through an osmotic mini-pump at 2.5 mg/kg per day beginning 3 days before moderate transverse aortic constriction or sham surgery. Calpeptin administration blocked both calpain enrichment and myocardial cell death in the 4-week PO beta3 mice. Because beta3 integrin contributes to cardioprotective signaling, these studies indicate that the loss of specific integrin function could be a key mechanism for calpain-mediated programmed cell death of cardiomyocytes in PO myocardium.
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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.