ArticleCell death and differentiation2016
Cardiac Gab1 deletion leads to dilated cardiomyopathy associated with mitochondrial damage and cardiomyocyte apoptosis.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Identification of Long Noncoding RNA by In Situ Hybridization Approaches.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Epithelial Gab1 Restricts Sepsis-Induced Intestinal Injury by Orchestrating TNF/NF-κB Axis.Mediators of inflammation · 2026Article
- SARM1 Exacerbates Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure by Enhancing NADFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Fine mapping of candidate effector genes for heart rate.Human genetics · 2024Article
- Global Proteomic Analysis Reveals Alterations in Differentially Expressed Proteins between Cardiopathic Lamin A/C Mutations.Journal of proteome research · 2024Article
- Gab1 Overexpression Attenuates Susceptibility to Ventricular Arrhythmias in Pressure Overloaded Heart Failure Mouse Hearts.Cardiovascular drugs and therapy · 2024Article
- Review
- An extensive β1-adrenergic receptor gene signaling network regulates molecular remodeling in dilated cardiomyopathies.JCI insight · 2023Article
- Epithelial Gab1 calibrates RIPK3-dependent necroptosis to prevent intestinal inflammation.JCI insight · 2023Article
- Cardiac-Specific Expression of Cre Recombinase Leads to Age-Related Cardiac Dysfunction Associated with Tumor-like Growth of Atrial Cardiomyocyte and Ventricular Fibrosis and Ferroptosis.International journal of molecular sciences · 2023Article
- Self-assembly of DNA nanostructure containing cell-specific aptamer as a precise drug delivery system for cancer therapy in non-small cell lung cancer.Journal of nanobiotechnology · 2022Article
- SIRT6 Mitigates Heart Failure With Preserved Ejection Fraction in Diabetes.Circulation research · 2022Article
- Multiple-model machine learning identifies potential functional genes in dilated cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Mitochondria in Pathological Cardiac Hypertrophy Research and Therapy.Frontiers in cardiovascular medicine · 2021Review
- S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression.Molecular medicine reports · 2021Article
- Akt Inhibition Enhanced the Growth Inhibition Effects of Low-Dose Heavy-Ion RadiationFrontiers in oncology · 2021Article
- Advances in the role and mechanism of BAG3 in dilated cardiomyopathy.Heart failure reviews · 2021Review
- LncRNA PVT1 Promotes Hypoxia-Induced Cardiomyocyte Injury by Inhibiting miR-214-3p.BioMed research international · 2021Article
- Differential gene responses 3 days following infarction in the fetal and adolescent sheep heart.Physiological genomics · 2020Article
- Characterisation of the developing heart in a pressure overloaded model utilising RNA sequencing to direct functional analysis.Journal of anatomy · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
A vital step in the development of heart failure is the transition from compensatory cardiac hypertrophy to decompensated dilated cardiomyopathy (DCM) during cardiac remodeling under mechanical or pathological stress. However, the molecular mechanisms underlying the development of DCM and heart failure remain incompletely understood. In the present study, we investigate whether Gab1, a scaffolding adaptor protein, protects against hemodynamic stress-induced DCM and heat failure. We first observed that the protein levels of Gab1 were markedly reduced in hearts from human patients with DCM and from mice with experimental viral myocarditis in which DCM developed. Next, we generated cardiac-specific Gab1 knockout mice (Gab1-cKO) and found that Gab-cKO mice developed DCM in hemodynamic stress-dependent and age-dependent manners. Under transverse aorta constriction (TAC), Gab1-cKO mice rapidly developed decompensated DCM and heart failure, whereas Gab1 wild-type littermates exhibited adaptive left ventricular hypertrophy without changes in cardiac function. Mechanistically, we showed that Gab1-cKO mouse hearts displayed severe mitochondrial damages and increased cardiomyocyte apoptosis. Loss of cardiac Gab1 in mice impaired Gab1 downstream MAPK signaling pathways in the heart under TAC. Gene profiles further revealed that ablation of Gab1 in heart disrupts the balance of anti- and pro-apoptotic genes in cardiomyocytes. These results demonstrate that cardiomyocyte Gab1 is a critical regulator of the compensatory cardiac response to aging and hemodynamic stress. These findings may provide new mechanistic insights and potential therapeutic target for DCM and heart failure.
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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.