ArticleAnnals of the rheumatic diseases2016
AMP-activated protein kinase suppresses urate crystal-induced inflammation and transduces colchicine effects in macrophages.
Article in Annals of the rheumatic diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Systematic review of the subcutaneous air pouch model using monosodium urate and calcium pyrophosphate and recommendations for studying crystal-related arthropathies.Animal models and experimental medicine · 2025Pooled it
- Effects of colchicine in adults with metabolic syndrome: A pilot randomized controlled trial.Diabetes, obesity & metabolism · 2019Trial
- Potential mechanisms of natural products in improving gouty arthritis: Focusing on NLRP3 inflammasome regulation.Journal of pharmaceutical analysis · 2026Review
- Mechanisms and therapeutic potential of colchicine in atherosclerotic cardiovascular disease.Nature cardiovascular research · 2026Review
- Empagliflozin improves renal injury of diabetic nephropathy complicated with hyperuricemia through AMPK by promoting autophagy and inhibiting apoptosis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026Article
- Programmed cell death in gouty nephropathy: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Engineering nanoparticles for macrophage reprogramming in chronic inflammatory diseases: current advances, challenges, and future perspectives.Frontiers in bioengineering and biotechnology · 2026Review
- Targeting Inflammation in Type 2 Diabetes: The Role of Colchicine.Current diabetes reviews · 2026Review
- Targeted suppression of CCR7/NF-κB signaling by apoptotic body-inspired colchicine nanovesicles halts atherosclerotic progression.Journal of nanobiotechnology · 2025Article
- Gout and NLRP3 Inflammasome Biology.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Follow the Molecule from Crystal Arthropathy to Comorbidities: The 2024 G-CAN Gold Medal Award Awardee Lecture.Gout, urate, and crystal deposition disease · 2025Article
- The Role of Autophagy in HIV Infection and Immunological Recovery of ART-Treated PLWH.Viruses · 2025Review
- Elevated uric acid level and metabolic syndrome in Non-Hispanic Black American adults.Journal of diabetes and metabolic disorders · 2025Article
- Article
- Comprehensive Treatment of Gout with Traditional Chinese Medicine: A Modern Pathophysiological Perspective.International journal of general medicine · 2025Review
- gCTRP3 inhibits oophorectomy‑induced osteoporosis by activating the AMPK/SIRT1/Nrf2 signaling pathway in mice.Molecular medicine reports · 2024Article
- Emerging insights into the role of IL-1 inhibitors and colchicine for inflammation control in type 2 diabetes.Diabetology & metabolic syndrome · 2024Review
- Should Glucokinase be Given a Chance in Diabetes Therapeutics? A Clinical-Pharmacological Review of Dorzagliatin and Lessons Learned So Far.Clinical drug investigation · 2024Review
- [Colchicine alleviates myocardial ischemia-reperfusion injury in mice by activating AMPK].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Colchicine Blocks Abdominal Aortic Aneurysm Development by Maintaining Vascular Smooth Muscle Cell Homeostasis.International journal of biological sciences · 2024Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveAMP-activated protein kinase (AMPK) is metabolic biosensor with anti-inflammatory activities. Gout is commonly associated with excesses in soluble urate and in nutrition, both of which suppress tissue AMPK activity. Gout is driven by macrophage-mediated inflammation transduced partly by NLRP3 inflammasome activation and interleukin (IL)-1β release. Hence, we tested the hypothesis that AMPK activation limits monosodium urate (MSU) crystal-induced inflammation.
methodsWe studied bone marrow-derived macrophages (BMDMs) from AMPKα1 knockout and wild-type mice, and assessed the selective AMPK pharmacological activator A-769662 and a low concentration (10 nM) of colchicine. We examined phosphorylation (activation) of AMPKα Thr172, NLRP3 mRNA expression, and caspase-1 cleavage and IL-1β maturation using western blot and quantitative RT-PCR approaches. We also assessed subcutaneous murine air pouch inflammatory responses to MSU crystals in vivo.
resultsMSU crystals suppressed phosphorylation of AMPKα in BMDMs. Knockout of AMPKα1 enhanced, and, conversely, A-769662-inhibited MSU crystal-induced inflammatory responses including IL-1β and CXCL1 release in vitro and in vivo. A-769662 promoted AMPK-dependent macrophage anti-inflammatory M2 polarisation and inhibited NLRP3 gene expression, activation of caspase-1 and IL-1β. Colchicine, at low concentration (10 nM) achieved in gout flare prophylaxis dosing, promoted phosphorylation of AMPKα and macrophage M2 polarisation, and reduced activation of caspase-1 and release of IL-1β and CXCL1 by MSU crystals in BMDMs in vitro.
conclusionsAMPK activity limits MSU crystal inflammation in vitro and in vivo, and transduces multiple anti-inflammatory effects of colchicine in macrophages. Targeting increased and sustained AMPK activation in inflammatory cells merits further investigation for enhancing efficacy of prophylaxis and treatment of gouty inflammation.
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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.