Evidence mapPaperPMID 41807354Full record

ReviewCell death discovery2026

Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression.

Jie Li, Wenchao Xu, Jie Ju, Min Liu, Wenxu Wang, Min Cheng, Xiaoyun Zhang, Xiaodong Cui, Hao Chen

Abstract readReview
In one paragraph

Review in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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.

Jie Li *Department of Physiology & Pathophysiology, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China.
Wenchao Xu *Weifang Key Laboratory of Basic Research on Chronic Diseases and Stem Cell Therapy, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China.
Jie JuDepartment of Physiology, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China.
Min LiuDepartment of neurology, Sunshine Union Hospital, Weifang, Shandong, PR China.
Wenxu WangWeifang Key Laboratory of Basic Research on Chronic Diseases and Stem Cell Therapy, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China.
Min ChengWeifang Key Laboratory of Basic Research on Chronic Diseases and Stem Cell Therapy, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China.
Xiaoyun ZhangWeifang Key Laboratory of Basic Research on Chronic Diseases and Stem Cell Therapy, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China. zhangxiaoyun@sdsmu.edu.cn.ORCID http://orcid.org/0000-0003-0417-9557
Xiaodong CuiDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China. xiaodongcui@sdsmu.edu.cn.ORCID http://orcid.org/0000-0001-5023-4890
Hao ChenWeifang Key Laboratory of Basic Research on Chronic Diseases and Stem Cell Therapy, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, PR China. chenhao@sdsmu.edu.cn.ORCID http://orcid.org/0000-0001-6251-5833

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis constitutes the primary pathological basis for cardiovascular diseases. It most commonly develops at the branching and curved regions of blood vessels. The disturbed blood flow in these regions can generate oscillatory shear stress (OSS). Endothelial cells exposed to OSS progressively undergo a transformation into mesenchymal cells, a process known as endothelial-to-mesenchymal transition (EndMT). EndMT is a critical event in the development of atherosclerosis. OSS promotes the occurrence of EndMT through multiple pathways. This paper provides a comprehensive analysis of the phenomena and mechanisms of OSS-induced EndMT, offering theoretical insights into the pathogenic mechanisms of atherosclerosis and corresponding therapeutic strategies.

Identifiers

PMID41807354
PMCPMC13039374

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.