Evidence map›Paper›PMID 41047676›Full record

ArticleCurrent medicinal chemistry2026

LncRNA HYMAI Promotes Endothelial Cell Autophagy via miR-19a-3p/ ATG14 to Attenuate the Progression of Coronary Atherosclerotic Disease.

Shao Ouyang, Zhi-Xiang Zhou, Hui-Ting Liu, Kun Zhou, Zhong Ren, Huan Liu, Qian Xu, Zhaoyue Wang, Wenhao Xiong, Gaofeng Zeng and 1 more

Abstract read
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In one paragraph

Article in Current medicinal chemistry, 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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1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

11 authors.

Shao OuyangKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Zhi-Xiang ZhouKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Hui-Ting LiuKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Kun ZhouKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Zhong RenKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Huan LiuKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Qian XuKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Zhaoyue WangKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Wenhao XiongKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Gaofeng ZengKey Laboratory of Heart Failure Prevention & Treatment of Hengyang, Clinical Medicine Research Center of Arteriosclerotic Disease of Hunan Province, Department of Cardiovascular Medicine, Hengyang Medical School, The Second Affiliated Hospital, University of South China , Hunan, 421001, China.
Zhi-Sheng JiangKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.

Funding

Clinical Medical Technology Innovation Guide Project of Hunan Province 2021SK51712Key Scientific Research Project of Department of Education of Hunan Province 23A0318Medical and Health Joint Project of Hunan Natural Science Foundation 2025JJ81008National Key Research and Development Program of China 2019YFA0801601Natural Science Foundation of Hunan Province 2021JJ40485, 2023JJ60048, 2025JJ50657Research Project of University of South China nk2020106Science and Health Joint Project of Hunan Natural Science Foundation 2021JJ70110Scientific research project of Hunan Provincial Health Commission 20201945Special Funding for Construction of Innovative Provinces in Hunan Province 2020SK2105Special Funds for Science and Technology Plan Project of Hengyang 2019jh426001Special Funds for the Innovative Construction of Hunan Province 2020SK4010
6 · The paper itself

Abstract

backgroundCoronary atherosclerotic disease (CAD), clinically manifesting as progressive coronary atherosclerosis (As), involves endothelial cell (EC) dysfunction. HYMAI may contribute to atherogenesis by acting on ECs, but its regulation of endothelial injury and role in As pathogenesis remain unclear.

methodsHYMAI expression was assessed via PCR array in blood samples from healthy individuals, patients with premature coronary atherosclerotic disease (PCAD), and patients with mature coronary atherosclerotic disease (MCAD) (each group consisting of 4 males and 2 females). Using male ApoE-/- and LDLR-/- mice fed with a high-fat diet (HFD) to model As, we evaluated the effects of endothelial-specific HYMAI overexpression on aortic lesions. Autophagy and apoptosis were analyzed in ox-LDL-treated human coronary artery endothelial cells (HCAECs).

resultsHYMAI levels increased sequentially in healthy individuals, PCAD, and MCAD patients. In HFD-fed ApoE DISCUSSION: HYMAI upregulation counteracts ox-LDL-treated endothelial autophagic inhibition via the miR-19a-3p/ATG14 pathway, rescuing apoptosis and attenuating As in both in vivo and in vitro settings.

conclusionOur results demonstrated that HYMAI attenuated As progression in As mice and ox-LDL-treated HCAECs by enhancing endothelial autophagy through the miR-19a-3p/ATG14 axis. These findings establish HYMAI as a novel regulatory mechanism and provide a potential druggable target for As and CAD.

Indexed as

AutophagyAutophagy-Related ProteinsCoronary Artery DiseaseEndothelial CellsMicroRNAsRNA, Long NoncodingVesicular Transport ProteinsAdaptor Proteins, Vesicular TransportAnimalsApoptosisAtherosclerosisCells, CulturedDiet, High-FatDisease ProgressionFemaleHumansAdaptor Proteins, Vesicular TransportATG14 protein, humanAutophagy-Related ProteinsLipoproteins, LDLMicroRNAsMIR19A, humanoxidized low density lipoproteinRNA, Long NoncodingVesicular Transport ProteinsATG14atherosclerosisautophagycoronary atherosclerotic disease.HYMAImiR-19a-3p

Identifiers

PMID41047676

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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.