ArticleClinics (Sao Paulo, Brazil)2025
hsa_circ_0095812 accelerates periodontitis progression by adsorbing miR-485-3p-mediated THBS1 expression.
Article in Clinics (Sao Paulo, Brazil), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Clinical implications of dysregulated non-coding RNA expression in periodontitis: evidence synthesis from a systematic review and meta-analysis.Odontology · 2026Pooled it
- circMYO9B affects the progression of periodontitis by targeting the miR-4731-5p/USP15 axis.Journal of periodontal & implant science · 2026Article
- miR-671-5p as a diagnostic biomarker and therapeutic target in periodontitis via THBS1 regulation.Hereditas · 2025Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the role of hsa_circ_0095812 (circLRRC4C) in periodontitis and its mechanism with miR-485-3p and Thrombospondin-1 (THBS1).
methodsPeriodontal tissues were collected from periodontitis patients. Periodontal Ligament Cells (PDLCs) were stimulated with Lipopolysaccharide (LPS) and transfected. Cell viability, inflammation, apoptosis, and pyroptosis were analyzed. A mouse model of periodontitis was constructed and injected with a lentiviral plasmid vector targeting circLRRC4C. Immunohistochemistry was performed on the periodontal tissue of model mice. The relevant expression level of genes was measured via real-time reverse transcriptase-polymerase chain reaction or Western blot. The relationship between circLRRC4C and THBS1 with miR-485-3p was analyzed.
resultsCircLRRC4C was highly expressed in periodontitis tissues of patients and LPS-treated PDLCs. Downregulating circLRRC4C attenuated LPS-induced PDLC inflammation, apoptosis and pyroptosis and recovered cellular viability. CircLRRC4C acted as a sponge for miR-485-3p. CircLRRC4C affected LPS-induced PDLC apoptosis, pyroptosis and inflammation by regulating miR-485-3p. THBS1 was the target gene of miR-485-3p. Inhibition of THBS1 effectively improved LPS-induced periodontitis. CircLRRC4C aggravated LPS-induced PDLC apoptosis, pyroptosis and inflammation by regulating the miR-485-3p/THBS1 axis. Suppressing circLRRC4C effectively improved periodontitis in mice.
conclusionCircLRRC4C induces periodontitis progression by adsorbing miR-485-3p-mediated THBS1 expression.
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