Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Abnormal circ-CDK8 expression affects periodontitis development by regulating let-7b-5p/MAP4K3 signaling

Li Y., Yang C., Jin M., Liu T., Yuan C., Zheng J.

Laboratory Study on Ligament Injury, published in Regen Ther (2026) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Regen Ther (2026)
Reported sample size
—
Source database
Europe PMC
PMID
41716226
PMCID
PMC12914548
DOI
10.1016/j.reth.2026.101075

Abstract (original English)

Periodontitis, a chronic inflammatory disorder characterized by progressive alveolar bone loss, relies heavily on the osteogenic differentiation capacity of periodontal ligament stem cells for bone regeneration. While inflammatory conditions are known to impair this osteogenic potential, the specific regulatory mechanisms, particularly those involving circular RNAs, remain to be elucidated. This study was therefore conducted to investigate the functional role of circ-CDK8 in regulating periodontal ligament stem cells (PDLSCs) differentiation under inflammatory conditions and to elucidate its mechanism of action through the let-7b-5p/MAP4K3 pathway and associated autophagy processes. Our investigation revealed significant upregulation of circ-CDK8 in periodontitis tissues compared to healthy tissues. Using an inflammatory model with TNF-α and IL-1β stimulation, we demonstrated that circ-CDK8 suppression enhanced osteogenic differentiation while concurrently reducing autophagic activity. Mechanistic studies established that circ-CDK8 executes its regulatory function through the let-7b-5p/MAP4K3 axis, where its inhibition promotes osteogenic differentiation via autophagy modulation. These findings not only identify a novel circ-CDK8/let-7b-5p/MAP4K3 regulatory pathway in periodontitis pathogenesis but also position circ-CDK8 as a promising therapeutic target for periodontal regene

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research