ArticleNature metabolism2021
Colchicine acts selectively in the liver to induce hepatokines that inhibit myeloid cell activation.
Article in Nature metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- A systematic review of the neuroprotective role and biomarker potential of GDF15 in neurodegeneration.Frontiers in immunology · 2024Pooled it
- Trial
- Drug-Drug Interactions and the Clinical Tolerability of Colchicine Among Patients With COVID-19: A Secondary Analysis of the COLCORONA Randomized Clinical Trial.JAMA network open · 2024Trial
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- AAV-NRF2 protects retinal and choroidal vasculature in a GDF15-dependent manner in an oxidative damage model of AMD.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dynamic microtubules as sensors in animal cells.Biophysical journal · 2026Review
- Colchicine attenuates kidney injury by modulating the NLRP3 inflammasome pathway.Molecular medicine (Cambridge, Mass.) · 2026Article
- Mechanisms and therapeutic potential of colchicine in atherosclerotic cardiovascular disease.Nature cardiovascular research · 2026Review
- Improving Laboratory-Based Cancer Drug Discovery Study Designs for Better Research Translations.Methods and protocols · 2026Review
- A GDF-15-GFRAL axis controls autoimmune T cell responses during neuroinflammation.Nature immunology · 2026Article
- Colchicine Alleviates Non-Atherosclerotic Vascular Aging by Targeting Endothelial Dysfunction and Inflammatory Status.Journal of inflammation research · 2026Article
- A Trifluoromethyl Quinazoline Compound Regulates the Epithelial-Mesenchymal Transition of Prostatic Hyperplasia Cells by Inhibiting the Secretion of TGF-β1 in Stromal Cells.Current issues in molecular biology · 2025Article
- Peritumoral colonic epithelial cell-derived GDF15 sustains colorectal cancer via regulation of glycolysis and histone lactylation.Nature aging · 2025Article
- Cigarette smoke extract promotes metastasis and oxaliplatin resistance in colon adenocarcinoma through GDF15/ERBB2/AKT pathway.European journal of medical research · 2025Article
- Cardiac adaptation to endurance exercise training requires suppression of GDF15 via PGC-1α.Nature cardiovascular research · 2025Article
- Metabolic Messenger: growth differentiation factor 15.Nature metabolism · 2025Review
- Colchicine-BODIPY Probes: Evidence for the Involvement of Intracellular Membranes in the Targeting of Colchicine to Tubulin.ACS pharmacology & translational science · 2025Article
- The Role of NLRP3 Inflammasome in Type 2 Diabetes Mellitus and Its Macrovascular Complications.Journal of clinical medicine · 2025Review
- The inflammatory endotype in osteoarthritis: Reflections from the 2024 OARSI clinical trials symposium (CTS) with a special emphasis on feasibility for clinical development.Osteoarthritis and cartilage open · 2025Review
- Exploring Anti-Inflammatory Treatment as Upstream Therapy in the Management of Atrial Fibrillation.Journal of clinical medicine · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Colchicine has served as a traditional medicine for millennia and remains widely used to treat inflammatory and other disorders. Colchicine binds tubulin and depolymerizes microtubules, but it remains unclear how this mechanism blocks myeloid cell recruitment to inflamed tissues. Here we show that colchicine inhibits myeloid cell activation via an indirect mechanism involving the release of hepatokines. We find that a safe dose of colchicine depolymerizes microtubules selectively in hepatocytes but not in circulating myeloid cells. Mechanistically, colchicine triggers Nrf2 activation in hepatocytes, leading to secretion of anti-inflammatory hepatokines, including growth differentiation factor 15 (GDF15). Nrf2 and GDF15 are required for the anti-inflammatory action of colchicine in vivo. Plasma from colchicine-treated mice inhibits inflammatory signalling in myeloid cells in a GDF15-dependent manner, by positive regulation of SHP-1 (PTPN6) phosphatase, although the precise molecular identities of colchicine-induced GDF15 and its receptor require further characterization. Our work shows that the efficacy and safety of colchicine depend on its selective action on hepatocytes, and reveals a new axis of liver-myeloid cell communication. Plasma GDF15 levels and myeloid cell SHP-1 activity may be useful pharmacodynamic biomarkers of colchicine action.
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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.