ArticleJACC. Basic to translational science2023
TAK1 Activation by NLRP3 Deficiency Confers Cardioprotection Against Pressure Overload-Induced Cardiomyocyte Pyroptosis and Hypertrophy.
Article in JACC. Basic to translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- S-Adenosylmethionine-Dependent Methylation, Protein Arginine Methyltransferases and Cardiovascular Diseases.Biomolecules · 2026Review
- LTBP4 deficiency inhibits NLRP3 inflammasome activation in cardiomyocytes and attenuates heart failure in male mice.Nature communications · 2026Article
- Leveraging the shared and opposing genetic mechanisms in the heritable cardiomyopathies.Research square · 2026Article
- A Brief Description of the Cellular Mechanisms Involved in Cardiac Chemical Hypoxia.Cardiovascular toxicology · 2026Review
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years.Mechanobiology in medicine · 2025Review
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Vessel-On-A-Chip Coupled Proteomics Reveal Pressure-Overload-Induced Vascular Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Protosappanin A protects against pathological cardiac hypertrophy by inhibiting oxidative stress and NLRP3 inflammasome-mediated pyroptosis via activation of the Nrf2 signaling pathway.Frontiers in cardiovascular medicine · 2025Article
- A multi-omics approach identifies the key role of disorders of sphingolipid metabolism in Ang II-induced hypertensive cardiomyopathy myocardial remodeling.Scientific reports · 2024Article
- Pyroptosis in health and disease: mechanisms, regulation and clinical perspective.Signal transduction and targeted therapy · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Deletion of Interleukin-1β Converting Enzyme Alters Mouse Cardiac Structure and Function.Biology · 2024Article
- Tit for TAK1: Reciprocal Regulation of Inflammasome Signaling in Cardiac Hypertrophy.JACC. Basic to translational science · 2023Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A comprehensive view of the role of NLRP3/caspase-1/GSDMD-mediated pyroptosis in pressure overload cardiac hypertrophy is presented in this study. Furthermore, mitigation of NLRP3 deficiency-induced pyroptosis confers cardioprotection against pressure overload through activation of TAK1, whereas this salutary effect is abolished by inhibition of TAK1 activity, highlighting a previously unrecognized reciprocally regulatory role of NLRP3-TAK1 governing inflammation-induced cell death and hypertrophic growth. Translationally, this study advocates strategies based on inflammation-induced cell death might be exploited therapeutically in other inflammatory and mechanical overload disorders, such as myocardial infarction and mitral regurgitation.
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