Evidence map›Paper›PMID 40597276›Full record

ArticleCell communication and signaling : CCS2025

ACPA-Induced ATP release and K

Li Cai, Kai Zhang, Jian Gao, Bing Xiao, Meng Li, Xiangyun Meng, Zhipeng Chen, Xiaoling Chen, Shixian Chen, Juan Li

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  4. Review
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  7. Article
  8. Review
  9. Review
  10. Myocardial infarction in rheumatic diseases.Rheumatology international · 2025
    Review
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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

10 authors.

Li Cai *Department of Nephrology and Rheumatology, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, China.
Kai Zhang *Nanjing Hospital of Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Jian Gao *Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Bing Xiao *The First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Meng LiDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiangyun MengDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhipeng ChenThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Xiaoling ChenThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Shixian ChenDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China. shixian@smu.edu.cn.
Juan LiDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China. lijuan@smu.edu.cn.

Funding

National Natural Science Foundation of China 82304928National Natural Science Foundation of China 82374206
6 · The paper itself

Abstract

objectivesAnti-citrullinated protein antibodies (ACPA) is one of the key inducers of the initiation and maintenance of the immune-inflammatory response in Rheumatoid arthritis (RA), yet evidence is lacking on how ACPA drives the inflammatory response.

methodsCitrullinated collagen-induced arthritis (C-CIA) were performed to evaluate the inflammatory response, especially NLRP3 inflammasome activation, in ACPA + arthritis model. Macrophages differentiated from THP-1 cell line were stimulated by ACPA purified from RA patients' serum, and the localization and interaction of molecules involved in NLRP3 inflammasome were analyzed by confocal microscopy and immunoprecipitation.

resultsMice with arthritis induced by citrullinated collagen showed higher levels of ACPA and enhanced activation of the NLRP3 inflammasome. This was evidenced by increased levels of IL-1β in the peripheral blood and more pronounced pyroptosis and caspase-1 (p20) expression in the synovial tissue, compared to mice induced with common collagen. ACPA induced overactivation of NLRP3 inflammasome in THP-1-differentiated macrophages in vitro. ACPA recruits SFK kinase by binding to integrin α

conclusionOur study demonstrates that ACPA can trigger both the priming and activation of the NLRP3 inflammasome. This process involves the release of ATP and the efflux of K

Indexed as

Adenosine TriphosphateAnti-Citrullinated Protein AntibodiesArthritis, RheumatoidInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinPotassiumAnimalsConnexinsHumansMacrophagesMaleMiceTHP-1 CellsAdenosine TriphosphateAnti-Citrullinated Protein AntibodiesConnexinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinPotassiumAnti-citrullinated protein antibodyATPK+ effluxMacrophagesNLRP3 inflammasomeRheumatoid arthritis

Identifiers

PMID40597276
PMCPMC12210964

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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.