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ArticleApplied biochemistry and biotechnology2026

Long Non-coding RNA Taurine Up-regulated Gene 1 Exacerbates Cardiac Fibrosis and Cardiomyocyte Apoptosis After Acute Myocardial Infarction by Modulating the MicroRNA-27a-3p/Zinc-finger Protein 36 Axis.

Shuai Ji, XinChao Ma, Yu He

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Article in Applied biochemistry and biotechnology, 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

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3 authors.

Shuai JiDepartment of Cardiovascular Medicine, Henan Provincial Chest Hospital, Ward 7, No. 1 Weiwu Road, Zhengzhou City, 450008, Henan Province, China. star-tear3@gzhmu-edu.cn.ORCID http://orcid.org/0000-0003-3844-5868
XinChao MaDepartment of Cardiovascular Medicine, Henan Provincial Chest Hospital, Ward 7, No. 1 Weiwu Road, Zhengzhou City, 450008, Henan Province, China.
Yu HeThe Second School of Clinical Medicine, Southern Medical University, GuangzhouCity, 510515, Guangdong Province, China.

Funding

Joint Co-construction Project of Medical Science and Technology Tackling Program in Henan Province No. LHGJ20490738
6 · The paper itself

Abstract

purposeIncreasing data supports the significant involvement of both long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in the pathogenesis of acute myocardial infarction (AMI). This study intends to explore the role of lncRNA Taurine up-regulated gene 1 (TUG1) in cardiac fibrosis and cardiomyocyte apoptosis in AMI via modulating the miR-27a-3p/Zinc-finger protein 36 (ZFP36) axis.

methodsA myocardial infarction (MI) mouse model was established by ligating the left anterior descending coronary artery. The mice were injected with the vectors correspondingly. Cardiac function, myocardial tissue pathology, cardiomyocyte apoptosis, and cardiac fibrosis were assessed. Mouse cardiomyocyte line HL-1 cells after hypoxia treatment were transfected, and cell proliferation and apoptosis were analyzed. The relationship between TUG1, miR-27a-3p and ZFP36 was tested.

resultsLevels of TUG1 and ZFP36 were elevated, while the level of miR-27a-3p level was reduced in MI mice and hypoxia-treated HL-1 cells. Myocardial fibrosis and cardiomyocyte apoptosis were alleviated in MI mice after decreasing TUG1 or increasing miR-27a-3p. In cell experiments, knockdown of TUG1 or overexpression of miR-27a-3p reduced cardiomyocyte apoptosis and promoted proliferation. Inhibition of miR-27a-3p attenuated the effects of TUG1 downregulationin vivoandin vitro. TUG1 acted as a sponge for miR-27a-3p, which targeted ZFP36. Up-regulation of ZFP36 counteracted the effects of miR-27a-3p overexpression in hypoxic HL-1 cells.

conclusionTUG1 exacerbates cardiac fibrosis and cardiomyocyte apoptosis after AMI via the miR-27a-3p/ZFP36 axis.

Indexed as

ApoptosisMicroRNAsMyocardial InfarctionMyocytes, CardiacRNA, Long NoncodingAnimalsCell LineFibrosisMaleMiceMice, Inbred C57BLUp-Regulationlong non-coding RNA TUG1, mouseMicroRNAsMirn27 microRNA, mouseRNA, Long NoncodingAcute myocardial infarctionApoptosisFibrosisMicroRNA-27a-3pTaurine up-regulated gene 1Zinc-finger protein 36

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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.