ArticleJournal of cellular and molecular medicine2021
MicroRNA-302c-3p inhibits endothelial cell pyroptosis via directly targeting NOD-, LRR- and pyrin domain-containing protein 3 in atherosclerosis.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Guanxinshu attenuates atherosclerosis by suppressing Galectin-3-mediated NLRP3 inflammasome activation.Journal of molecular histology · 2026Article
- Decoding the molecular mechanisms of pyroptosis and its therapeutic development prospects.Frontiers in cell and developmental biology · 2026Review
- Mapping Current Studies of tRNA Fragments onto Disease Landscape.Biomolecules · 2025Review
- A review on NLRP3 inflammasome modulation by animal venom proteins/peptides: mechanisms and therapeutic insights.Inflammopharmacology · 2025Review
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
- MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction.International journal of molecular sciences · 2024Article
- Bone marrow mesenchymal stem cellsderived exosomes stabilize atherosclerosis through inhibiting pyroptosis.BMC cardiovascular disorders · 2023Article
- Review
- CRISPR/Cas9 therapeutics: progress and prospects.Signal transduction and targeted therapy · 2023Review
- Integrated analysis of the lncRNA-miRNA-mRNA network based on competing endogenous RNA in atrial fibrillation.Frontiers in cardiovascular medicine · 2023Article
- Recent advances in targeted delivery of non-coding RNA-based therapeutics for atherosclerosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- MiR-130a-5p contributed to the progression of endothelial cell injury by regulating FAS.European journal of histochemistry : EJH · 2022Article
- Gasdermin D Deficiency Limits the Transition of Atherosclerotic Plaques to an Inflammatory Phenotype inBiomedicines · 2022Article
- The regulatory roles of aminoacyl-tRNA synthetase in cardiovascular disease.Molecular therapy. Nucleic acids · 2021Review
- Inflammatory Mechanisms Contributing to Endothelial Dysfunction.Biomedicines · 2021Review
- Expression profiles and potential roles of transfer RNA-derived small RNAs in atherosclerosis.Journal of cellular and molecular medicine · 2021Article
- The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development.Journal of cellular and molecular medicine · 2021Review
- MicroRNA-302c-3p inhibits endothelial cell pyroptosis via directly targeting NOD-, LRR- and pyrin domain-containing protein 3 in atherosclerosis.Journal of cellular and molecular medicine · 2021Article
- Autophagy, Pyroptosis, and Ferroptosis: New Regulatory Mechanisms for Atherosclerosis.Frontiers in cell and developmental biology · 2021Review
- miR-153-3p Targets βII Spectrin to Regulate Formaldehyde-Induced Cardiomyocyte Apoptosis.Frontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation and endothelial dysfunction are important participants and drivers in atherosclerosis. NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation and the resulting pyroptosis are involved in the initiation and vicious circle of chronic inflammation, thus playing an indispensable role in atherosclerosis. Accordingly, blocking the activation of NLRP3 inflammasome may be a promising treatment strategy to blunt the progression of atherosclerosis. In this study, it was demonstrated that miR-302c-3p exerted anti-pyroptosis effects by directly targeting NLRP3 in vivo and in vitro. In brief, the expression of miR-302c-3p was down-regulated whereas the expression of NLRP3 was up-regulated in human plaques and in vitro pyroptosis model of endothelial cells. Overexpression of miR-302c-3p suppressed endothelial cell pyroptosis by targeting specific sites of NLRP3. By comparison, down-regulation of endogenous miR-302c-3p led to the opposite results, which were reversed by silencing the expression of NLRP3. Finally, the up-regulation of miR-302c-3p inhibited the inflammation and pyroptosis of atherosclerosis mouse model. In conclusion, miR-302c-3p may be a powerful and attractive target for suppressing endothelial inflammation and pyroptosis, providing a novel strategy for preventing or alleviating the progression of atherosclerosis.
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Registered trials
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