ArticleBMC cardiovascular disorders2024
Colchicine ameliorates myocardial injury induced by coronary microembolization through suppressing pyroptosis via the AMPK/SIRT1/NLRP3 signaling pathway.
Article in BMC cardiovascular disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 16 citations in OpenAlex.
- The Central Role of the AMPK/SIRT1/PGC-1α Signaling Axis in Skeletal Muscle Physiology and Pathology and Its Targeted Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Role of NLRP3 Inflammasome Inhibitors in Endothelial Dysfunction and Vascular Repair.Antioxidants (Basel, Switzerland) · 2026Review
- Colchicine attenuates kidney injury by modulating the NLRP3 inflammasome pathway.Molecular medicine (Cambridge, Mass.) · 2026Article
- Colchicine in Cardiovascular Disease: Evidence Structure, Clinical Efficacy, Safety, and Translational Positioning Across Cardiovascular Syndromes.International journal of molecular sciences · 2026Review
- Semaglutide ameliorates coronary microembolization-induced injury by suppressing apoptosis and inflammation via the HMGB1/RAGE/NF-κB p65 pathway.Journal of geriatric cardiology : JGC · 2026Article
- Quercetin attenuates ferroptosis-associated myocardial injury in rats after coronary microembolization by activating the Nrf2/HO-1 signaling pathway.Iranian journal of basic medical sciences · 2026Article
- Exercise Alleviates Atherosclerosis Through the Modulation of the NLRP3 Inflammasome.Current molecular medicine · 2026Review
- Dapagliflozin ameliorates kidney injury following limb ischemia-reperfusion via the AMPK/SIRT1/NLRP3 pathway.Renal failure · 2025Article
- AMPK/SIRT1/PGC-1α Signaling Pathway: Molecular Mechanisms and Targeted Strategies From Energy Homeostasis Regulation to Disease Therapy.CNS neuroscience & therapeutics · 2025Review
- Targeting the NLRP3 inflammasome with natural products for ischemia-reperfusion injury across organs: mechanisms, structure-activity relationships, and delivery innovations.Inflammopharmacology · 2025Review
- Vericiguat reduces pyroptosis in rats with coronary microembolization by inhibiting the AMPK/Nrf2/NLRP3 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- Efficacy of Colchicine in Reducing NT-proBNP, Caspase-1, TGF-β, and Galectin-3 Expression and Improving Echocardiography Parameters in Acute Myocardial Infarction: A Multi-Center, Randomized, Placebo-Controlled, Double-Blinded Clinical Trial.Journal of clinical medicine · 2025Article
- Precise photopharmacological eradication of metastatic tumor cells.Disease models & mechanisms · 2025Article
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
- The critical role of Sirt1 in ischemic stroke.Frontiers in pharmacology · 2025Review
- Research Progress of Regulatory Cell Death in Coronary Microembolization.International journal of medical sciences · 2025Review
- Identification of new potent NLRP3 inhibitors by multi-level in-silico approaches.BMC chemistry · 2024Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCoronary microembolization(CME)is a common complication in acute coronary syndrome and percutaneous coronary intervention, which is closely related to poor prognosis. Pyroptosis, as an inflammatory programmed cell death, has been found to be associated with CME-induced myocardial injury. Colchicine (COL) has potential benefits in coronary artery disease due to its anti-inflammatory effect. However, the role of colchicine in pyroptosis-related CME-induced cardiomyocyte injury is unclear. This study was carried out to explore the effects and mechanisms of colchicine on myocardial pyroptosis induced by CME.
methodsThe CME animal model was constructed by injecting microspheres into the left ventricle with Sprague-Dawley rats, and colchicine (0.3 mg/kg) pretreatment seven days before and on the day of modeling or compound C(CC)co-treatment was given half an hour before modeling. The study was divided into 4 groups: Sham group, CME group, CME + COL group, and CME + COL + CC group (10 rats for each group). Cardiac function, serum myocardial injury markers, myocardial histopathology, and pyroptosis-related indicators were used to evaluate the effects of colchicine.
resultsColchicine pretreatment improved cardiac dysfunction and reduced myocardial injury induced by CME. The main manifestations were the improvement of left ventricular systolic function, the decrease of microinfarction area, and the decrease of mRNA and protein indexes related to pyroptosis. Mechanistically, colchicine increased the phosphorylation level of adenosine monophosphate-activated protein kinase (AMPK), promoted the expression of silent information regulation T1 (SIRT1), and inhibited the expression of NOD-like receptor pyrin containing 3 (NLRP3) to reduce myocardial pyroptosis. However, after CC co-treatment with COL, the effect of colchicine was partially reversed.
conclusionColchicine improves CME-induced cardiac dysfunction and myocardial injury by inhibiting cardiomyocyte pyroptosis through the AMPK/SIRT1/NLRP3 signaling pathway.
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