ArticleJournal of diabetes investigation2020
Activation of autophagy inhibits nucleotide-binding oligomerization domain-like receptor protein 3 inflammasome activation and attenuates myocardial ischemia-reperfusion injury in diabetic rats.
Article in Journal of diabetes investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Pirfenidone restores metabolic hormones and cardiac autophagy via p-AMPK in MASH.Journal of translational medicine · 2026Article
- Platelet-rich plasma alleviates skin photoaging by activating autophagy and inhibiting inflammasome formation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Elevated novel inflammatory markers in heart failure patients are associated with increased risk of adverse outcomes within one year: insights from a longitudinal study.Frontiers in cardiovascular medicine · 2025Article
- Article
- The role of the NLRP3 inflammasome and pyroptosis in cardiovascular diseases.Nature reviews. Cardiology · 2024Review
- The mechanism by which miR-494-3p regulates PGC1-α-mediated inhibition of mitophagy in cardiomyocytes and alleviation of myocardial ischemia-reperfusion injury.BMC cardiovascular disorders · 2023Article
- Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023Review
- Nrf2 protects against myocardial ischemia-reperfusion injury in diabetic rats by inhibiting Drp1-mediated mitochondrial fission.Open medicine (Warsaw, Poland) · 2023Article
- cPKCγ Deficiency Exacerbates Autophagy Impairment and Hyperphosphorylated Tau Buildup through the AMPK/mTOR Pathway in Mice with Type 1 Diabetes Mellitus.Neuroscience bulletin · 2022Article
- Targeting the NLRP3 inflammasome in cardiovascular diseases.Pharmacology & therapeutics · 2022Review
- [Down-regulation of SIK2 expression alleviates myocardial ischemia-reperfusion injury in rats by inhibiting autophagy through the mTOR-ULK1 signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review).Experimental and therapeutic medicine · 2022Review
- The role of autophagy in death of cardiomyocytes.Journal of molecular and cellular cardiology · 2022Review
- Role of NLRP3 Inflammasome in Myocardial Ischemia-Reperfusion Injury and Ventricular Remodeling.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- The Role of NLRP3 Inflammasome Signaling on Arrhythmias in Diabetes.Journal of inflammation research · 2022Review
- Interaction Between Autophagy andFrontiers in cellular and infection microbiology · 2022Review
- Leptin Induces Apoptotic and Pyroptotic Cell Death via NLRP3 Inflammasome Activation in Rat Hepatocytes.International journal of molecular sciences · 2021Article
- Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia.Military Medical Research · 2021Article
- Inhibited HDAC3 or Elevated MicroRNA-494-3p Plays a Protective Role in Myocardial Ischemia-Reperfusion Injury via Suppression of BRD4.Molecular neurobiology · 2021Article
- The Interplay between Autophagy and NLRP3 Inflammasome in Ischemia/Reperfusion Injury.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
AIMS/
introductionDiabetic hearts are more vulnerable to ischemia-reperfusion injury (I/RI). The activation of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome can mediate the inflammatory process, and hence might contribute to myocardial I/RI. Activation of autophagy can eliminate excess reactive oxygen species and alleviate myocardial I/RI in diabetes. The present study aimed to investigate whether the activation of autophagy can alleviate diabetic myocardial I/RI through inhibition of NLRP3 inflammasome activation. MATERIALS AND
methodsA dose of 65 mg/kg streptozotocin was given by tail vein injection to establish a type 1 diabetes model in the rats. The left anterior descending coronary artery was ligated for 30 min followed by reperfusion for 2 h to establish a myocardial I/RI model. H9C2 cardiomyocytes were exposed to high glucose (33 mmol/L) and subjected to hypoxia-reoxygenation (6 h hypoxia followed by 4 h reoxygenation).
resultsThe diabetic rats showed significant inhibition of cardiac autophagy (decreased LC3-II/I and increased p62) that was concomitant with increased activation of NLRP3 inflammasome (increased NLRP3, apoptosis-related spots protein cleaved caspase-1, interleukin-18, interleukin-1β) and more severe myocardial I/RI (elevated creatine kinase myocardial band, lactate dehydrogenase and larger infarct size). However, administration of rapamycin, an inhibitor of the autophagy, to activate autophagy resulted in the inhibition of NLRP3 inflammasome, and finally alleviated myocardial I/RI. In vitro, high glucose inhibited autophagy, while activating NLRP3 inflammasome in H9C2 cardiomyocytes and aggravating hypoxia-reoxygenation injury, but rapamycin reversed these adverse effects of high glucose.
conclusionActivation of autophagy can suppress the formation of NLRP3 inflammasome, which in turn attenuates myocardial ischemia-reperfusion injury in diabetic rats.
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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.