Evidence map›Paper›PMID 39446285›Full record

ArticleCurrent medical science2024

Porphyromonas gingivalis Induces Chronic Kidney Disease through Crosstalk between the NF-κB/NLRP3 Pathway and Ferroptosis in GMCs.

Xue Li, Chao Yao, Dong-Mei Lan, Yan Wang, Sheng-Cai Qi

Abstract read
PubMed Publisher
In one paragraph

Article in Current medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Xue LiMedical College, Anhui University of Science and Technology, Huainan, 232007, China.
Chao YaoDepartment of Oral Prosthodontics, Shanghai Stomatological Hospital, Fudan University, Shanghai, 200001, China.
Dong-Mei LanDepartment of Oral Prosthodontics, Shanghai Stomatological Hospital, Fudan University, Shanghai, 200001, China.
Yan WangMedical College, Anhui University of Science and Technology, Huainan, 232007, China. kq_wangyan@fudan.edu.cn.
Sheng-Cai QiMedical College, Anhui University of Science and Technology, Huainan, 232007, China. qishengcai@fudan.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePorphyromonas gingivalis (P.gingivalis) is a gram-negative bacterium found in the human oral cavity and is a recognized pathogenic bacterium associated with chronic periodontitis and systemic diseases, including chronic kidney disease (CKD), but the roles and molecular mechanism of P.gingivalis in CKD pathogenesis are unclear.

methodsIn this study, an animal model of oral P.gingivalis administration and glomerular mesangial cells (GMCs) cocultured with M1-polarized macrophages and P.gingivalis supernatant were constructed. After seven weeks of P.gingivalis gavaged, peripheral blood was collected to detect the changes in renal function. By collecting the teeth and kidneys of mice, H&E staining and IHC were used to analyze the expression of periodontal inflammatory factors in mice, PAS staining was used to analyze glomerular lesions. The supernatant of macrophages was treated with 5% P.gingivalis supernatant. H&E staining, IHC, Western blot and RT-PCR were applied to analyze renal inflammatory factors, macrophage M1 polarization, NF-κB, NLRP3 and ferroptosis changes in vitro.

resultsWe found that oral P.gingivalis administration induced CKD in mice. P.gingivalis supernatant induced macrophage polarization and inflammatory factor upregulation, which triggered the activation of the NF-κB/NLRP3 pathway and ferroptosis in GMCs. By inhibiting the NF-κB/NLRP3 pathway and ferroptosis in GMCs, cell viability and the inflammatory response were partially alleviated in vitro.

conclusionWe demonstrated that P.gingivalis induced CKD in mice by triggering crosstalk between the NF κB/NLRP3 pathway and ferroptosis in GMCs. Overall, our study suggested that periodontitis can promote the pathogenesis of CKD in mice, which provides evidence of the importance of periodontitis therapy in the prevention and treatment of CKD. P.gingivalis promotes ferroptosis in kidneys and accelerates the progression of CKD through NF-κB/NLRP3 signaling pathway.

Indexed as

FerroptosisMacrophagesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPorphyromonas gingivalisRenal Insufficiency, ChronicSignal TransductionAnimalsBacteroidaceae InfectionsDisease Models, AnimalHumansMaleMesangial CellsMiceNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousechronic kidney diseaseferroptosisglomerular mesangial cellsmacrophagesNF-κB/NLRP3 pathwayPorphyromonas gingivalis

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.