Evidence map›Paper›PMID 42409783›Full record

ArticleCell death discovery2026

Regulation of acute myocardial infarction by CircTMCC1 through mitochondrial dysfunction and AMPK/mTOR-driven M1 macrophage polarization: role in QFR assessment.

Mengmeng Ren, Shu He, Mengyang Duan, Boyu Chi, Zhiyuan Chen, Zhenyu Zhao, Zhongga Ciren, Yangzong Qiangba, Yahong Fu, Gaochao Wang and 3 more

Abstract read
In one paragraph

Article in Cell death discovery, 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
–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

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

13 authors.

Mengmeng RenDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Shu He *Department of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mengyang Duan *Department of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Boyu ChiDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhiyuan ChenDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhenyu ZhaoDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhongga CirenDepartment of Cardiovascular Medicine, Lhasa People's Hospital, Lhasa, China.
Yangzong QiangbaDepartment of Cardiovascular Medicine, Lhasa People's Hospital, Lhasa, China.
Yahong FuDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Gaochao WangChangzhou Hospital to Nanjing University of Chinese Medicine, Changzhou, China.
Liang YuanDepartment of Cardiovascular Medicine, Chongqing Hospital of Jiangsu Province Hospital, Chongqing, China.
Fenghui AnDepartment of Critical Care Medicine, The Friendship Hospital of Ili Kazakh Autonomous Prefecture, Yining, China. anfenghui.1975@163.com.
Enzhi JiaDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. enzhijia@njmu.edu.cn.ORCID http://orcid.org/0000-0003-1354-9855

Funding

National Natural Science Foundation of China (National Science Foundation of China) 8117018
6 · The paper itself

Abstract

Circular RNAs (circRNAs) have been implicated in various cardiovascular diseases and hold promise as diagnostic biomarkers and therapeutic targets. However, the roles and mechanisms of circRNAs in coronary artery disease (CAD) and its severe complication, acute myocardial infarction (AMI), remain unclear. CircRNA sequencing, fluorescence in situ hybridization, and quantitative PCR were used to assess circTMCC1 expression in human coronary artery segments, peripheral blood mononuclear cells (PBMCs) from CAD patients, M1 macrophages, and an AMI mouse model. Multiple analytical methods were employed to investigate the predictive value of circTMCC1 for quantitative flow ratio (QFR) measurements. In vitro, we employed plasmid overexpression, small interfering RNA transfection, flow cytometry, immunofluorescence, reactive oxygen species (ROS), and mitochondrial membrane potential assays. In vivo, Masson's trichrome, hematoxylin and eosin staining, and immunohistochemistry were performed. Mechanistic investigations included bioinformatics, RNA pull-down, RNA immunoprecipitation, co-immunoprecipitation, western blotting, and immunofluorescence. CircTMCC1 was significantly upregulated in CAD patients (p < 0.001) and associated with poor prognosis in AMI mouse models. CircTMCC1 was highly expressed in M1 macrophages (p < 0.001), and silencing its expression reduced M1 polarization, improved cardiac function after infarction, and regulated mitochondrial autophagy. Mechanistically, circTMCC1 facilitates the interaction between annexin A1 and the E3 ligase TRIM38, leading to annexin A1 degradation. Additionally, the AMPK/mTOR signaling pathway was identified as a downstream target of circTMCC1. These findings suggest that circTMCC1 may serve as a promising diagnostic biomarker and therapeutic target for CAD and AMI, potentially improving prognosis.

Identifiers

PMID42409783
PMCPMC13620124

What Socratic holds

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Registered trials

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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 Socratic graph.