Evidence map›Paper›PMID 38872145›Full record

ArticleCell communication and signaling : CCS2024

Mitochondrial DNA release via the mitochondrial permeability transition pore activates the cGAS-STING pathway, exacerbating inflammation in acute Kawasaki disease.

Ke Wei, Tao Chen, Hao Fang, Xianjuan Shen, Zhiyuan Tang, Jianmei Zhao

Abstract read
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Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

33 citing papers in PubMed.

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  10. Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  11. [cGAS-STING signaling pathway in Kawasaki disease: mechanistic insights and advances in clinical applications].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Review
  12. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors.

Ke Wei *Department of Pediatrics, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China.
Tao Chen *Department of Pediatrics, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China.
Hao FangDepartment of Pediatrics, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China.
Xianjuan ShenDepartment of Clinical Laboratory, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China.
Zhiyuan TangDepartment of Pharmacy, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China. tina2951@sina.com.
Jianmei ZhaoDepartment of Pediatrics, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China. zjmheart@163.com.

Funding

Graduate Practice Innovation Program of Jiangsu Province SJCX23_1802Jiangsu Provincial Commission of Health and Family Planning ZDA2020010Jiangsu Provincial Medical Association SYH-32034-0082Maternal and Child Health Project of Jiangsu Provincial Health Commission F202154Multi-centre Clinical Collaborative Research Project at Affiliated Hospital of Nantong University LCYJ-A06Nantong Municipal Health Commission 14th Five-Year Plan Innovation Team NTCXTD43National Natural Science Foundation of China 82270528People's Livelihood Science and Technology Projetct of Nantong Science and Technology Bureau MS22022116
6 · The paper itself

Abstract

backgroundKawasaki disease (KD) is an immune vasculitis of unknown origin, characterized by transient inflammation. The activation of the cGAS-STING pathway, triggered by mitochondrial DNA (mtDNA) release, has been implicated in the onset of KD. However, its specific role in the progression of inflammation during KD's acute phase remains unclear.

methodsWe measured mtDNA and 2'3'-cGAMP expression in KD patient serum using RT-qPCR and ELISA. A murine model of KD was induced by injecting Lactobacillus casei cell wall extract (LCWE), after which cGAS-STING pathway activation and inflammatory markers were assessed via immunohistochemistry, western blot, and RT-qPCR. Human umbilical vein endothelial cells (HUVECs) were treated with KD serum and modulators of the cGAS-STING pathway for comparative analysis. Mitochondrial function was evaluated using Mitosox staining, mPTP opening was quantified by fluorescence microscopy, and mitochondrial membrane potential (MMP) was determined with JC-1 staining.

resultsKD patient serum exhibited increased mtDNA and 2'3'-cGAMP expression, with elevated levels of pathway-related proteins and inflammatory markers observed in both in vivo and in vitro models. TEM confirmed mitochondrial damage, and further studies demonstrated that inhibition of mPTP opening reduced mtDNA release, abrogated cGAS-STING pathway activation, and mitigated inflammation.

conclusionThese findings indicate that mtDNA released through the mPTP is a critical activator of the cGAS-STING pathway, contributing significantly to KD-associated inflammation. Targeting mtDNA release or the cGAS-STING pathway may offer novel therapeutic approaches for KD management.

Indexed as

DNA, MitochondrialInflammationMembrane ProteinsMitochondrial Permeability Transition PoreMucocutaneous Lymph Node SyndromeNucleotidyltransferasesSignal TransductionAcute DiseaseAnimalsChild, PreschoolCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseFemaleHumansHuman Umbilical Vein Endothelial CellsMaleMicecGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialMembrane ProteinsMitochondrial Permeability Transition PoreNucleotidyltransferasesSTING1 protein, humanSTING ProteincGAS-STING pathwayKawasaki diseasemPTPmtDNA

Identifiers

PMID38872145
PMCPMC11177463

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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.