ArticleBioscience reports2021
MicroRNA-543-3p down-regulates inflammation and inhibits periodontitis through KLF6.
Article in Bioscience reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Trust in Context: A Three-Factor Experimental Study.Behavioral sciences (Basel, Switzerland) · 2026Article
- KLF6 activation marks an angiogenic and apoptosis resistant endothelial phenotype in pulmonary arterial hypertension.Communications biology · 2026Article
- Psychological mechanisms of work responsibility among Chinese university administrative staff: the roles of organizational identification, burnout, and role conflict.Frontiers in psychology · 2026Article
- Advances in the roles and mechanisms of mesenchymal stem cell derived microRNAs on periodontal tissue regeneration.Stem cell research & therapy · 2024Review
- Ropinirole suppresses LPS-induced periodontal inflammation by inhibiting the NAT10 in an ac4C-dependent manner.BMC oral health · 2024Article
- Silencing KLF6 Alleviates Cigarette Smoke Extract-Induced Mitochondrial Dysfunction in Bronchial Epithelial Cells by SIRT4 Upregulation.International journal of chronic obstructive pulmonary disease · 2024Article
- Anti-apoptosis and anti-inflammation activity of circ_0097010 downregulation in lipopolysaccharide-stimulated periodontal ligament cells by miR-769-5p/Krüppel like factor 6 axis.Journal of dental sciences · 2023Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-543-3p (miR-543-3p) has been reported to be involved in many human disease's progression, but its role in inflammation is still unclear. After bacterial infection, innate immune cells are activated to trigger inflammation by recognizing lipopolysaccharide (LPS) on the bacterial outer membrane. In our research, it showed that miR-543-3p was down-regulated in LPS-treated periodontal ligament cells (PDLCs). And it mediated the apoptosis of PDLC induced by LPS, which may be involved in periodontitis development. Besides, up-regulation of miR-543-3p alleviated the inflammatory damage induced by LPS. Furthermore, our research demonstrated Kruppel-like factor 6 (KLF6) served as a direct downstream target of miR-543-3p to play a vital role in periodontitis. Simply put, these findings suggest that miR-543-3p could down-regulate inflammation and inhibit periodontitis by targeting KLF6, and it provides a new insight into the molecular mechanism of periodontitis, which may be helpful for the early diagnosis and treatment of this disease.
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Registered trials
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