ArticleThe Journal of clinical investigation2022
TAB2 deficiency induces dilated cardiomyopathy by promoting RIPK1-dependent apoptosis and necroptosis.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 43 citations in OpenAlex.
- Xinmailong Injection Attenuates Doxorubicin-Induced Chronic Heart Failure by Regulating the SIRT1/Caspase-3 Axis and Metabolic Reprogramming: An Integrative Network Pharmacology and Metabolomics Study.Current medical science · 2026Article
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- TAB2 Causes Neuronal Damage by Aggravating Microglia-Mediated Neuroinflammation in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Autoantibody-Based Models for the Diagnosis and Activity Assessment of Takayasu Arteritis.Journal of cardiovascular translational research · 2026Article
- The dual role of RIPK family in IBD: from cell death to therapeutic targeting.Molecular medicine (Cambridge, Mass.) · 2026Review
- Identification of diagnostic and therapeutic roles of programmed cell death-related proteins in dilated cardiomyopathy: a multi-omics and experimental validation study.Scientific reports · 2026Article
- Loss of DNA methyltransferase 3a enhances Caspase-8 transcription and promotes cardiomyocyte pyroptosis during myocardial infarction.Nature communications · 2026Article
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Genome-wide association study of atopic and autoimmune comorbidities in alopecia areata.Frontiers in immunology · 2026Article
- CPNE5 overexpression inhibits cardiomyocytes apoptosis by promoting the degradation of FAS receptor.iScience · 2025Article
- New insights into pulmonary arterial hypertension: interaction between PANoptosis and perivascular inflammatory responses.Apoptosis : an international journal on programmed cell death · 2025Review
- Review
- TAB2 deficiency induces dilated cardiomyopathy by promoting mitochondrial calcium overload in human iPSC-derived cardiomyocytes.Molecular medicine (Cambridge, Mass.) · 2025Article
- Article
- Prognostic signature and therapeutic drug identification for dilated cardiomyopathy based on necroptosis via bioinformatics and experimental validation.Scientific reports · 2025Article
- Kuoxin Decoction Alleviated Left Ventricular Remodeling by Inhibiting Cardiomyocyte Apoptosis Through ASK1/JNK/Cx43 Signaling Pathway in cTnTR141W Transgenic Mice and in vitro.Drug design, development and therapy · 2025Article
- Targeted Delivery of Exosome-Derived miRNA-185-5p Inhibitor via Liposomes Alleviates Apoptosis and Cuproptosis in Dilated Cardiomyopathy.International journal of nanomedicine · 2025Article
- USP53 Drives Ethanol-Induced Myocardial Injury by Promoting K63 Deubiquitination-Dependent RIPK1 Activation at K377.Research (Washington, D.C.) · 2025Article
- Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation.Antioxidants (Basel, Switzerland) · 2024Review
- Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in TGF-β-activated kinase 1 binding protein 2 (TAB2) have been implicated in the pathogenesis of dilated cardiomyopathy and/or congenital heart disease in humans, but the underlying mechanisms are currently unknown. Here, we identified an indispensable role for TAB2 in regulating myocardial homeostasis and remodeling by suppressing receptor-interacting protein kinase 1 (RIPK1) activation and RIPK1-dependent apoptosis and necroptosis. Cardiomyocyte-specific deletion of Tab2 in mice triggered dilated cardiomyopathy with massive apoptotic and necroptotic cell death. Moreover, Tab2-deficient mice were also predisposed to myocardial injury and adverse remodeling after pathological stress. In cardiomyocytes, deletion of TAB2 but not its close homolog TAB3 promoted TNF-α-induced apoptosis and necroptosis, which was rescued by forced activation of TAK1 or inhibition of RIPK1 kinase activity. Mechanistically, TAB2 critically mediates RIPK1 phosphorylation at Ser321 via a TAK1-dependent mechanism, which prevents RIPK1 kinase activation and the formation of RIPK1-FADD-caspase-8 apoptotic complex or RIPK1-RIPK3 necroptotic complex. Strikingly, genetic inactivation of RIPK1 with Ripk1-K45A knockin effectively rescued cardiac remodeling and dysfunction in Tab2-deficient mice. Together, these data demonstrated that TAB2 is a key regulator of myocardial homeostasis and remodeling by suppressing RIPK1-dependent apoptosis and necroptosis. Our results also suggest that targeting RIPK1-mediated cell death signaling may represent a promising therapeutic strategy for TAB2 deficiency-induced dilated cardiomyopathy.
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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.