ArticleThe Journal of biological chemistry2013
Talin1 has unique expression versus talin 2 in the heart and modifies the hypertrophic response to pressure overload.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 88 citations in OpenAlex.
- ALY688 Protects Against Myocardial Ischemia-Reperfusion Injury via Direct Effects and Rab8a-Dependent Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
- Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025Review
- Identification of anoikis-related genes in heart failure: bioinformatics and experimental validation.Hereditas · 2025Article
- Inhibition of Talin2 dedifferentiates myofibroblasts and reverses lung and kidney fibrosis.Scientific reports · 2025Article
- Logic-based modeling of biological networks with Netflux.PLoS computational biology · 2025Article
- Novel Multiplexed Plasma Biomarker Panel Has Diagnostic and Prognostic Potential in Children With Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2024Article
- Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024Article
- Cardiomyocyte external mechanical unloading activates modifications of α-actinin differently from sarcomere-originated unloading.The FEBS journal · 2023Article
- Article
- Comparative proteomic analysis of glomerular proteins in IgA nephropathy and IgA vasculitis with nephritis.Clinical proteomics · 2023Article
- Genome Editing and Pathological Cardiac Hypertrophy.Advances in experimental medicine and biology · 2023Article
- Characterization of focal adhesion proteins in rodent hepatic stellate cells.Histochemistry and cell biology · 2022Article
- Loss of talin in cardiac fibroblasts results in augmented ventricular cardiomyocyte hypertrophy in response to pressure overload.American journal of physiology. Heart and circulatory physiology · 2022Article
- Article
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Identification of atrial-enriched lncRNA Walras linked to cardiomyocyte cytoarchitecture and atrial fibrillation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- To detect potential pathways and target genes in infantile Pompe patients using computational analysis.BioImpacts : BI · 2022Article
- Striated muscle proteins are regulated both by mechanical deformation and by chemical post-translational modification.Biophysical reviews · 2021Review
- Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms.International journal of molecular sciences · 2021Review
- Review
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Integrins are adhesive, signaling, and mechanotransduction proteins. Talin (Tln) activates integrins and links it to the actin cytoskeleton. Vertebrates contain two talin genes, tln1 and tln2. How Tln1 and Tln2 function in cardiac myocytes (CMs) is unknown. Tln1 and Tln2 expression were evaluated in the normal embryonic and adult mouse heart as well as in control and failing human adult myocardium. Tln1 function was then tested in the basal and mechanically stressed myocardium after cardiomyocyte-specific excision of the Tln1 gene. During embryogenesis, both Tln forms are highly expressed in CMs, but in the mature heart Tln2 becomes the main Tln isoform, localizing to the costameres. Tln1 expression is minimal in the adult CM. With pharmacological and mechanical stress causing hypertrophy, Tln1 is up-regulated in CMs and is specifically detected at costameres, suggesting its importance in the compensatory response to CM stress. In human failing heart, CM Tln1 also increases compared with control samples from normal functioning myocardium. To directly test Tln1 function in CMs, we generated CM-specific Tln1 knock-out mice (Tln1cKO). Tln1cKO mice showed normal basal cardiac structure and function but when subjected to pressure overload showed blunted hypertrophy, less fibrosis, and improved cardiac function versus controls. Acute responses of ERK1/2, p38, Akt, and glycogen synthase kinase 3 after mechanical stress were strongly blunted in Tln1cKO mice. Given these results, we conclude that Tln1 and Tln2 have distinct functions in the myocardium. Our data show that reduction of CM Tln1 expression can lead to improved cardiac remodeling following 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.