ReviewCell & bioscience2025
Molecular mechanisms of endothelial-mesenchymal transition and its pathophysiological feature in cerebrovascular disease.
Review in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed.
- Beyond EMT: Mesenchymal drift as an emerging driver of stromal-immune reprogramming in prostate cancer.iScience · 2026Review
- Single-cell Technologies in Atherosclerosis: Uncovering Cellular Heterogeneity, Mechanisms, and Therapeutic Opportunities.Current atherosclerosis reports · 2026Review
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- NRG1 Suppresses NLRP3 Inflammasome Activation and Endothelial-Mesenchymal Transition in Cerebral Ischemia-Reperfusion Injury: Association with the AKT/NF-κB Pathway.Journal of inflammation research · 2026Article
- Non-Coding RNAs in Obesity-Driven Vascular Dysfunction: Mechanisms, EndMT, and Translational Opportunities.Chonnam medical journal · 2026Review
- Inhibitory Effect of Sirtuin6 on EndMT by Regulating Oxidative Stress and Autophagy in Coxsackievirus B3-Induced Cardiac Endothelial Cells.Immunity, inflammation and disease · 2025Article
- Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The phenomenon of endothelial-mesenchymal transition (EndMT), a distinct subtype of epithelial-mesenchymal transition (EMT), has garnered significant attention from scholars. EndMT refers to the process whereby endothelial cells (ECs) transform into mesenchymal cells in response to various stimuli, resulting in the loss of their original characteristics. This process has diverse implications in both physiological and pathological states. Under physiological conditions, EndMT plays a crucial role in the development of the cardiovascular system. Conversely, under pathological conditions, EndMT has been identified as a pivotal factor in the development of cardiovascular diseases. Nonetheless, a comprehensive overview of EndMT in cerebrovascular disease is currently lacking. Here, we discuss the heterogeneity of EndMT occurrence and the regulatory factors involved in its development and analyze the feasibility of EndMT as a therapeutic target, aiming to provide a solid theoretical foundation and evidence to address diseases caused by pathological EndMT.
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What OpenQuestion holds
Registered trials
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.