Evidence map›Paper›PMID 40598260›Full record

ArticleJournal of translational medicine2025

Remdesivir inhibits endothelial activation and atherosclerosis by coupling TAL1 to TRAF6.

Hanning Zhang, Ruru Li, Qianqian Huo, Li Li, Min Li, Shunxin Hu, Changjie Ren, Zongyin Wu, Chenghu Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Hanning Zhang *Shandong First Medical University, Jinan, China.
Ruru Li *Shandong First Medical University, Jinan, China.
Qianqian HuoDepartment of Cardiology, Jining First People's Hospital, Shandong First Medical University, No. 6 Jiankang Road, Jining, 272000, Shandong, China.
Li LiDepartment of Cardiology, Jining First People's Hospital, Shandong First Medical University, No. 6 Jiankang Road, Jining, 272000, Shandong, China.
Min LiDepartment of Cardiology, Jining First People's Hospital, Shandong First Medical University, No. 6 Jiankang Road, Jining, 272000, Shandong, China.
Shunxin HuShandong First Medical University, Jinan, China.
Changjie RenDepartment of Cardiology, Jining First People's Hospital, Shandong First Medical University, No. 6 Jiankang Road, Jining, 272000, Shandong, China.
Zongyin WuDepartment of Cardiology, Jining First People's Hospital, Shandong First Medical University, No. 6 Jiankang Road, Jining, 272000, Shandong, China. wuzysp@163.com.
Chenghu ZhangDepartment of Cardiology, Jining First People's Hospital, Shandong First Medical University, No. 6 Jiankang Road, Jining, 272000, Shandong, China. zchjnyy2020@163.com.ORCID 0009-0002-6277-3466

Funding

National Natural Science Foundation of China 82100485Natural Science Foundation of Shandong Province ZR2024QH024
6 · The paper itself

Abstract

backgroundAtherosclerosis is characterized by complex pathological processes, including endothelial dysfunction and inflammation. The underlying pathogenic mechanisms have been well elucidated; however, effective treatments are yet to be validated. Our study explored the novel application of a recognized antiviral agent, remdesivir, focusing on its impact on endothelial activation and atherosclerosis.

methodsPharmacological treatment with remdesivir significantly reduced atherosclerotic lesions in the total aorta and decreased VCAM-1 expression in aortic roots of ApoE-/- mice. Remdesivir notably attenuated ox-LDL-induced endothelial cell (EC) activation, monocyte adhesion, and ROS production. In HUVECs, TAL1 interference via siRNA significantly increased TRAF6 protein levels, which was reversed by remdesivir. Remdesivir also reduced both total and K63-linked ubiquitination of TRAF6 in HUVECs. Immunoprecipitation assays revealed diminished co-localization of the two proteins under ox-LDL treatment, but this effect was reversed by remdesivir. Importantly, ectopic adeno-associated virus (AAV)-mediated overexpression of TAL1 reduced atherosclerotic lesions and VCAM-1 expression in the aorta of ApoE-/- mice.

resultsIn ApoE

conclusionsRemdesivir impedes atherosclerosis progression by re-establishing the interaction between TAL1 and TRAF6, diminishing endothelial activation. These findings offer an innovative therapeutic approach for atherosclerosis.

Indexed as

Adenosine MonophosphateAlanineAtherosclerosisBasic Helix-Loop-Helix ProteinsEndothelial CellsTNF Receptor-Associated Factor 6AnimalsAortaApolipoproteins ECell AdhesionHumansHuman Umbilical Vein Endothelial CellsLipoproteins, LDLMaleMiceMice, Inbred C57BLAdenosine MonophosphateAlanineApolipoproteins EBasic Helix-Loop-Helix ProteinsLipoproteins, LDLoxidized low density lipoproteinReactive Oxygen SpeciesremdesivirTNF Receptor-Associated Factor 6Vascular Cell Adhesion Molecule-1

Identifiers

PMID40598260
PMCPMC12220244

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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 OpenQuestion graph.