Evidence map›Paper›PMID 42113414›Full record

ArticleJournal of thrombosis and thrombolysis2026

CircRNA_0007444 modulates cardiomyocyte inflammation and apoptosis induced by myocardial ischemia-reperfusion injury via miR-16-5p/MFN2.

Zhaoxia Teng, Lijing Fan, Sheng Li, Zhuo Lv, Yihao Wang

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Article in Journal of thrombosis and thrombolysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

5 authors.

Zhaoxia Teng *Qingdao Municipal Hospital (Qingdao Geriatric Hospital), Qingdao, 266000, China.
Lijing Fan *Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Sheng LiDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210000, China.
Zhuo LvDepartment of Cardiology, General Hospital of the Yangtze River Shipping, Wuhan, 430015, China.
Yihao WangCardiovascular Medicine Department, Pingliang Second People's Hospital, No. 79, East Street, Kongtong District, Pingliang City, 744000, Gansu, China. yihaowangdr@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischemia-reperfusion injury (MIRI) seriously affects myocardial function, with circular RNA's mechanism in MIRI under exploration. This study seeks to elucidate the clinical value and function of circRNA_0007444 in MIRI. The levels of circRNA_0007444 in the serum of 94 non-MIRI patients and 80 MIRI patients were compared. The clinical significance of circRNA_0007444 was evaluated from the perspectives of differentiating MIRI patients and identifying independent risk factors for MIRI. In vitro experiments, a hypoxia/reoxygenation (H/R)-induced human cardiomyocytes AC16 cell model was used to evaluate the regulatory effects of circRNA_0007444 on cell viability, apoptosis, myocardial injury and inflammation. In mechanism, the downstream miRNAs and target genes of circRNA_0007444 were predicted, and the participation of miR-16-5p and MFN2 was evaluated through the recovery experiment. Decreasing circRNA_0007444 could discriminate MIRI patients and severs as an independent risk factor for MIRI onset. CircRNA_0007444 was negatively correlated with myocardial injury indicators. In AC16 cells, H/R induced significant downregulation of circRNA_0007444, suppressed cell viability, promoted cell apoptosis, enhanced inflammation, and induced myocardial injury. Promoting circRNA_0007444 could protect AC16 cells from H/R-induced injury. CircRNA_0007444 could target and negatively regulate miR-16-5p. miR-16-5p could target and negatively regulate MFN2. The overexpression of miR-16-5p could reverse the protective effect of circRNA_0007444 overexpressing, while overexpression of MFN2 could eliminate this effect. circRNA_0007444 can be used as a biomarker for the early screening and identification of independent risk factors of MIRI. Promoting circRNA_0007444 could alleviate H/R-induced AC16 cell injury through the miR-16-5p/MFN2 axis.

Indexed as

ApoptosisGTP PhosphohydrolasesInflammationMicroRNAsMitochondrial ProteinsMyocardial Reperfusion InjuryMyocytes, CardiacRNA, CircularCell LineFemaleHumansMaleMiddle AgedGTP PhosphohydrolasesMicroRNAsMIRN16 microRNA, humanMitochondrial ProteinsRNA, CircularcircRNA_0007444InflammationMFN2miR-16-5pMyocardial ischemia-reperfusion injury

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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.