ArticleThe American journal of pathology2001
Disruption of integrin function in the murine myocardium leads to perinatal lethality, fibrosis, and abnormal cardiac performance.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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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
32 citing papers in PubMed, 103 citations in OpenAlex.
- ArfGAP with Dual Pleckstrin Homology Domains 2 Promotes Hypertrophy of Cultured Neonatal Cardiomyocytes.International journal of molecular sciences · 2025Article
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Targeting integrin pathways: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2023Review
- Altered intercellular communication and extracellular matrix signaling as a potential disease mechanism in human hypertrophic cardiomyopathy.Scientific reports · 2022Article
- Common and Distinctive Intercellular Communication Patterns in Human Obstructive and Nonobstructive Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Article
- Integrins in cardiac hypertrophy: lessons learned from culture systems.ESC heart failure · 2021Review
- Nicotinamide riboside kinase-2 alleviates ischemia-induced heart failure through P38 signaling.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Reduced myocyte complex N-glycosylation causes dilated cardiomyopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Mapping Heart Development in Flies: Src42A Acts Non-Autonomously to Promote Heart Tube Formation in Drosophila.Veterinary sciences · 2017Article
- Integrins as Therapeutic Targets for Respiratory Diseases.Current molecular medicine · 2015Review
- Integrins in development and cancer.Biophysical reviews · 2014Review
- ErbB/integrin signaling interactions in regulation of myocardial cell-cell and cell-matrix interactions.Biochimica et biophysica acta · 2013Review
- A computational approach to understand phenotypic structure and constitutive mechanics relationships of single cells.Annals of biomedical engineering · 2013Article
- Membrane-associated matrix proteolysis and heart failure.Circulation research · 2013Review
- The contribution of cellular mechanotransduction to cardiomyocyte form and function.Biomechanics and modeling in mechanobiology · 2012Article
- NOX2-derived reactive oxygen species are crucial for CD29-induced pro-survival signalling in cardiomyocytes.Cardiovascular research · 2012Article
- Changes in the myocardial interstitium and contribution to the progression of heart failure.Heart failure clinics · 2012Review
- Intercellular and extracellular mechanotransduction in cardiac myocytes.Pflugers Archiv : European journal of physiology · 2011Review
- Cardiac myocyte remodeling mediated by N-cadherin-dependent mechanosensing.American journal of physiology. Heart and circulatory physiology · 2011Article
- Heterogeneity in MT1-MMP activity with ischemia-reperfusion and previous myocardial infarction: relation to regional myocardial function.American journal of physiology. Heart and circulatory physiology · 2010Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The molecular mechanisms that regulate the cardiac hypertrophic response and the progression from compensated hypertrophy to decompensated heart failure have not been thoroughly defined. Alteration in cardiac extracellular matrix is a distinguishing characteristic of these pathological processes. Integrins, cell surface receptors that mediate cellular adhesion to the extracellular matrix, are signaling molecules that possess mechanotransduction properties. Therefore, we hypothesized that integrins are likely candidates to play an important role in cardiac function. To test this hypothesis, transgenic mice were constructed in which normal integrin function was disrupted by expression of a chimeric molecule encoding the transmembrane and extracellular domains of the Tac subunit of the IL-2 receptor, fused to the cytoplasmic domain of beta(1A) integrin (Tacbeta(1A)). Using the alpha myosin heavy chain promoter to target expression of this chimera to the cardiac myocyte, transgenic mice were generated that had varied levels of transgene expression. Multiple transgenic founders that expressed the transgene at high levels, died perinatally and exhibited replacement fibrosis. Lines that survived showed 1) hypertrophic changes concordant with reduction in endogenous beta(1) integrin levels, or 2) reduced basal contractility and relaxation as well as alterations in components of integrin signaling pathways. These data support an important role for beta(1) integrin in normal cardiac function.
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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.