ArticleScientific reports2019
Transcription modulation by CDK9 regulates inflammatory genes and RIPK3-MLKL-mediated necroptosis in periodontitis progression.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- HEATR1 deficiency enhanced gastric cancer cell PANoptosis to boost anti-tumor immunity.Molecular medicine (Cambridge, Mass.) · 2026Article
- Article
- c-FLIP as a master regulator of immune homeostasis and disease mechanisms.Cell death & disease · 2026Review
- Interplay between survival and regulated cell death mechanisms during periodontitis progression: a systematic review.The Japanese dental science review · 2025Review
- PANoptosis-related gene APAF1 may contribute to the progression of sepsis.Irish journal of medical science · 2025Article
- Emerging regulated cell death mechanisms in bone remodeling: decoding ferroptosis, cuproptosis, disulfidptosis, and PANoptosis as therapeutic targets for skeletal disorders.Cell death discovery · 2025Review
- Immunologic cell deaths: involvement in the pathogenesis and intervention therapy of periodontitis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Hallmarks of Periodontitis.Current medicinal chemistry · 2025Review
- An injectable and thermosensitive hydrogel with nano-aided NIR-II phototherapeutic and chemical effects for periodontal antibacteria and bone regeneration.Journal of nanobiotechnology · 2023Article
- Identification of hub cuproptosis related genes and immune cell infiltration characteristics in periodontitis.Frontiers in immunology · 2023Article
- Novel necroptosis-related gene signature for predicting the prognosis of pancreatic adenocarcinoma.Aging · 2022Article
- Mixed lineage kinase domain-like pseudokinase-mediated necroptosis aggravates periodontitis progression.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Circulating miRNAs as Epigenetic Mediators of Periodontitis and Preeclampsia Association.Disease markers · 2022Article
- Identification of ferroptosis, necroptosis, and pyroptosis-associated genes in periodontitis-affected human periodontal tissue using integrated bioinformatic analysis.Frontiers in pharmacology · 2022Article
- Article
- PANoptosis: A New Insight Into Oral Infectious Diseases.Frontiers in immunology · 2021Review
- Myofiber necroptosis promotes muscle stem cell proliferation via releasing Tenascin-C during regeneration.Cell research · 2020Article
- Periodontitis-level butyrate-induced ferroptosis in periodontal ligament fibroblasts by activation of ferritinophagy.Cell death discovery · 2020Article
- Tensile force-induced PDGF-BB/PDGFRβ signals in periodontal ligament fibroblasts activate JAK2/STAT3 for orthodontic tooth movement.Scientific reports · 2020Article
- Effects of different curcumin concentrations on human periodontal ligament fibroblast adhesion and proliferation on periodontally involved root surfaces: In-vitro study.Journal of oral biology and craniofacial researchArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclin-dependent kinase 9 (CDK9), one crucial molecule in promoting the transition from transcription pausing to elongation, is a critical modulator of cell survival and death. However, the pathological function of CDK9 in bacterial inflammatory diseases has never been explored. CDK9 inhibition or knock-down attenuated Porphyromonas gingivalis-triggered inflammatory gene expression. Gene-expression microarray analysis of monocytes revealed that knock-down of CDK9 not only affected inflammatory responses, but also impacted cell death network, especially the receptor-interacting protein kinase 3 (RIPK3)-mixed lineage kinase domain-like (MLKL)-mediated necroptosis after P. gingivalis infection. Inhibition of CDK9 significantly decreased necroptosis with downregulation of both MLKL and phosphorylated MLKL. By regulating caspase-8 and cellular FLICE inhibitory protein (cFLIP), key molecules in regulating cell survival and death, CDK9 affected not only the classic RIPK1-RIPK3-mediated necroptosis, but also the alternate TIR-domain-containing adapter-inducing interferon-β-RIPK3-mediated necroptosis. CDK9 inhibition dampened pro-inflammatory gene production in the acute infection process in the subcutaneous chamber model in vivo. Moreover, CDK9 inhibition contributed to the decreased periodontal bone loss and inflammatory response induced by P. gingivalis in the periodontal micro-environment. In conclusion, by modulating the RIPK3-MLKL-mediated necroptosis, CDK9 inhibition provided a novel mechanism to impact the progress of bacterial infection in the periodontal milieu.
Indexed as
Identifiers
What OpenQuestion holds
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.