ArticleJournal of signal transduction2011
Integrins are the necessary links to hypertrophic growth in cardiomyocytes.
Article in Journal of signal transduction, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 47 citations in OpenAlex.
- The spectrum of pregnancy-induced cardiac remodeling: transitioning from healthy adaptive hypertrophy to peripartum cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Plasma Proteomic Profiling Reveals ITGA2B as A Key Regulator of Heart Health in High-altitude Settlers.Genomics, proteomics & bioinformatics · 2025Article
- Matrisome remodeling in the myocardium of hypertrophic cardiomyopathy; novel targets for molecular diagnostics.Frontiers in cell and developmental biology · 2025Review
- Focal Adhesion's Role in Cardiomyocytes Function: From Cardiomyogenesis to Mechanotransduction.Cells · 2024Review
- Cardiac Differentiation Promotes Focal Adhesions Assembly through Vinculin Recruitment.International journal of molecular sciences · 2023Article
- Integrins Increase Sarcoplasmic Reticulum Activity for Excitation-Contraction Coupling in Human Stem Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2022Article
- Multiomic analyses reveal enriched glycolytic processes in β-myosin heavy chain-expressed cardiomyocytes in early cardiac hypertrophy.Journal of molecular and cellular cardiology plus · 2022Article
- Integrinβ3 mediates the protective effects of soluble receptor for advanced glycation end-products during myocardial ischemia/reperfusion through AKT/STAT3 signaling pathway.Apoptosis : an international journal on programmed cell death · 2022Article
- State of Knowledge on Molecular Adaptations to Exercise in Humans: Historical Perspectives and Future Directions.Comprehensive Physiology · 2022Article
- Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of ventricular non-compaction.European heart journal · 2021Article
- 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
- Extracellular matrix-mediated cellular communication in the heart.Journal of molecular and cellular cardiology · 2016Review
- Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure.Cardiology research and practice · 2016Review
- Talin1 is required for cardiac Z-disk stabilization and endothelial integrity in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- The (dys)functional extracellular matrix.Biochimica et biophysica acta · 2015Review
- Intrinsic cardiomyopathy in Marfan syndrome: results from in-vivo and ex-vivo studies of the Fbn1C1039G/+ model and longitudinal findings in humans.Pediatric research · 2015Article
- Talin Is Required Continuously for Cardiomyocyte Remodeling during Heart Growth in Drosophila.PloS one · 2015Article
- Mechanosensing and Regulation of Cardiac Function.Journal of clinical & experimental cardiology · 2014Article
- Temporal changes in integrin-mediated cardiomyocyte adhesion secondary to chronic cardiac volume overload in rats.American journal of physiology. Heart and circulatory physiology · 2014Article
- Talin1 has unique expression versus talin 2 in the heart and modifies the hypertrophic response to pressure overload.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
To compensate for hemodynamic overload of the heart, an event which stretches the myocardium, growth and survival signaling are activated in cardiac muscle cells (cardiomyocytes). Integrins serve as the signaling receptors of cardiomyocytes responsible for mechanotransduction toward intracellular signaling. The main integrin heterodimers on the cardiomyocyte surface are α(5)β(1) and α(v)β(3), and elimination of either β(1) or β(3) integrins impedes pressure-induced hypertrophic signaling and leads to increased mortality. The growth signaling pathways downstream of β(1) and β(3) integrins are well characterized. However, new integrin pathways responsible for inhibiting apoptosis induced by hemodynamic overload are emerging. β(1) and β(3) integrins activate differential survival signaling, yet both integrins initiate survival signaling downstream of ubiquitination and the kinase pathway including phosphoinositol-3-kinase (PI3K)/Akt. Further characterization of these integrin-signaling mechanisms may lead to drug targets to prevent decompensation to heart failure.
Identifiers
What OpenQuestion holds
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.