Evidence map›Paper›PMID 41485097›Full record

ArticleRheumatology (Oxford, England)2026

Anti-mitochondrial M2 antibody links to cardiac involvement and immune-mediated inflammatory myopathy-like pathology in myositis.

Yiyun Pang, Lixi Zhang, Chen Yao, Shuang Zhou, Jie Pang, Lihua Duan, Juan Meng, Chen Yu, Chanyuan Wu, Chaojun Hu and 10 more

Abstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Yiyun PangDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID 0000-0002-4453-1626
Lixi ZhangDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID 0000-0002-3699-1585
Chen YaoRespiratory and Critical Care Medicine, Chinese PLA General Hospital, Beijing, China.
Shuang ZhouDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID 0000-0001-8694-8561
Jie PangRheumatology Department, Cangzhou Central Hospital, Heibei, China.
Lihua DuanDepartment of Rheumatology and Clinical Immunology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Juan MengDepartment of Rheumatology and Clinical Immunology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Chen YuDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Chanyuan WuDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Chaojun HuDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Jinzhi LaiDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Yanhong WangDepartment of Epidemiology and Bio-statistics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Mingwei TangDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Lin QiaoDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Dong XuDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID 0000-0002-6413-3043
Jiuliang ZhaoDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Xiaofeng ZengDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID 0000-0002-3883-2318
Zhuang TianDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Mengtao LiDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID 0000-0003-4252-2889
Qian WangDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID 0000-0002-4541-9898

Funding

Chinese National Key Technology R&D Program, Ministry of Science and Technology 2022YFC2504603Chinese National Key Technology R&D Program, Ministry of Science and Technology 2024YFC2510304
6 · The paper itself

Abstract

objectivesCardiac involvement in idiopathic inflammatory myopathies (IIM) is rare but potentially severe. Anti-mitochondrial M2 antibody (AMA-M2) has been implicated in cardiac involvement, but the association remains underexplored. This study aims to evaluate the clinical, pathological and prognostic features of AMA-M2 IIM.

methodsThis historic prospective cohort included IIM patients hospitalized at Peking Union Medical College Hospital between 2008 and 2020. Outcomes were prospectively collected through the Prospective Registry Of MyositIS (PROMIS) registry. Cox regression models were employed to identify risk factors of cardiac involvement and mortality.

resultsAmong 987 IIM patients, 55 (6%) were AMA-M2 positive. These patients exhibited higher rates of PM (56% vs 23.5%, P < 0.001), and elevated baseline gamma-glutamyl transferase (78.0 vs 35.0, P < 0.001) and alkaline phosphatase (85.0 vs 64.0, P < 0.001). Throughout disease courses, AMA-M2-positive patients had significantly higher rates of cardiac involvement (60% vs 12.9%, P < 0.001), including arrhythmias (56%), heart failure (44%) and pulmonary hypertension (31%). Some of the muscle biopsies showed features consistent with immune-mediated necrotizing myopathy, cardiac biopsies demonstrating structural degeneration with minimal inflammation and liver biopsies confirming early-stage primary biliary cholangitis (PBC). Multivariate Cox analysis identified AMA-M2 positivity as an independent risk factor for cardiac involvement (hazard ratio 3.156, P < 0.001). Despite frequent cardiac manifestations, long-term survival did not differ between AMA-M2-positive and -negative patients (mean survival: 103.9 months vs 98.0 months, P = 0.86).

conclusionAMA-M2 positivity defines an IIM subgroup with significant cardiac involvement and an immune-mediated inflammatory muscle histology, but not necessarily worse long-term survival. These findings highlight the need for early recognition and tailored management of AMA-M2 IIM.

Indexed as

AutoantibodiesHeart DiseasesMitochondriaMyositisAdultAgedFemaleHumansMaleMiddle AgedPrognosisProspective StudiesRegistriesRisk FactorsAutoantibodiesAMA-M2cardiac involvementidiopathic inflammatory myopathies

Identifiers

PMID41485097
PMCPMC12790821

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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.