ArticleInternational journal of biological sciences2019
Metformin Inhibits the NLRP3 Inflammasome via AMPK/mTOR-dependent Effects in Diabetic Cardiomyopathy.
Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 254 papers, 1 of them a synthesis that pooled it.
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Who cites it
254 citing papers in PubMed, 1 synthesis or guideline pooled it, 448 citations in OpenAlex.
- Progress in the treatment of diabetic cardiomyopathy, a systematic review.Pharmacology research & perspectives · 2024Pooled it
- Fenofibrate as an Adjunct Therapy for Ulcerative Colitis: Targeting Inflammation via SIRT1, NLRP3, and AMPK Pathways: A Randomized Controlled Pilot Study.Drug design, development and therapy · 2024Trial
- Rg1 activates the AMPK/mTOR-autophagy axis and inhibits the NOD-like receptor 3 inflammasome to alleviate pyroptosis in periodontal ligament fibroblasts.Odontology · 2026Article
- Inflammatory signalling in diabetic cardiomyopathy: molecular mechanisms and potential therapeutic strategies.Nature reviews. Cardiology · 2026Review
- Nanoparticle-Based Targeted Drug-Delivery Systems for Cardiomyopathy: Mechanisms and Therapeutic Advances.Molecules (Basel, Switzerland) · 2026Review
- Hyper-O-GlcNAcylation destabilizes ARC to unleash NLRP3-mediated pyroptosis in diabetic cardiomyopathy.Acta pharmacologica Sinica · 2026Article
- Fasudil Protects Against Diclofenac-Induced Hepatorenal and Gastric Injury via Modulation of ROCK/TLR4/SIRT1 Signaling and Preservation of Tight Junctions.Journal of xenobiotics · 2026Article
- Recombinant myonectin ameliorates sepsis‑induced cardiomyopathy by alleviating mitochondrial dysfunction via the AdipoR1/AMPK pathway.International journal of molecular medicine · 2026Article
- Injectable bioactive hydrogels as pharmacological drug delivery platforms for post-myocardial infarction cardiac repair: therapeutic cargo engineering, stimuli-responsive release mechanisms, and translational perspectives.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Regulation of acute myocardial infarction by CircTMCC1 through mitochondrial dysfunction and AMPK/mTOR-driven M1 macrophage polarization: role in QFR assessment.Cell death discovery · 2026Article
- Myeloid Cdc42 deficiency-mediated macrophage pyroptosis exacerbates diabetic cardiomyopathy in type 1 diabetes mellitus.Cardiovascular diabetology · 2026Article
- Metformin and cRGDfc-Modified Nanoparticles Loaded with Curcumin for Age-Related Macular Degeneration: In Vitro Pharmacodynamics and Molecular Mechanisms.Pharmaceutics · 2026Article
- AMPK-NLRP3 Inflammasome Crosstalk: Structural Insights, Molecular Mechanisms, and Therapeutic Implications for Inflammation and Neuroinflammation.Molecular neurobiology · 2026Review
- Cross-regulatory mechanisms linking ferroptosis, epigenetics, and circadian rhythm to mitochondrial quality control in diabetic cardiomyopathy.Journal of advanced research · 2026Review
- Reversing diastolic dysfunction in diabetes: a mitochondrial quality control-centric pharmacological approach.Acta diabetologica · 2026Review
- Metformin as a potential therapeutic agent in broken heart syndrome: Targeting AMPK-dependent cardio-protection and microvascular function.Molecular biology reports · 2026Review
- Loss of Peroxiredoxin 6 Drives Age-Related Klf9/NF-Antioxidants (Basel, Switzerland) · 2026Article
- Interconnected cell death pathways: central mechanisms and therapeutic targets in impaired follicular development of polycystic ovary syndrome.Journal of ovarian research · 2026Review
- Ulcerative colitis, pathophysiological mechanisms and drug repurposing: a new therapeutic dawn-narrative review.Inflammopharmacology · 2026Review
- Mitochondrial Homeostasis in Diabetic Cardiomyopathy: From Dysfunction to Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
194 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metformin is a widely used antidiabetic drug for type 2 diabetes that can play a cardioprotective role through multiple pathways. It is a recognized agonist of AMP-activated protein kinase (AMPK) that blocks mitochondrial complex I. The NLRP3 inflammasome has been demonstrated to be activated in diabetic cardiomyopathy (DCM). However, the role of metformin in regulating the NLRP3 signaling pathway in DCM remains unclear. It has been reported that AMPK can inhibit NLRP3 by activating autophagy. The aim of this study was to investigate whether metformin can inhibit the NLRP3 inflammasome by activating the AMPK/mTOR pathway in DCM. In this study, streptozotocin-induced C57BL/6 mice and high glucose-treated primary cardiomyocytes from neonatal mice were treated with metformin or an AMPK inhibitor compound C. Echocardiography, hematoxylin-eosin and Masson staining showed that the function and morphology of the diabetic hearts were improved after metformin treatment, whereas these parameters deteriorated after intervention with an AMPK inhibitor. Immunohistochemical staining, immunofluorescence staining and western blot assays indicated that the expression levels of mTOR, NLRP3, caspase-1, IL-1β and GSDMD-N were decreased in the diabetic model treated with metformin and were reversed after the administration of an AMPK inhibitor
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