ArticleScientific reports2025
The new perspective on understanding the mechanisms of cardiovascular diseases development.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Lipid-Induced Endothelial Dysfunction: Pro-Atherogenic Properties of Multinucleated Variant Endothelial Cells.International journal of molecular sciences · 2026Article
- Functional Differences Between Typical and Multinucleated Endothelial Cells Under Low-Density Lipoprotein Exposure.International journal of molecular sciences · 2026Article
- Integrative Analysis of VSMC, Macrophage, and Fibroblast Responses to LDLs in Aortic Pathologies.International journal of molecular sciences · 2026Article
- Development of a Nomogram to Classify In-Hospital Atrial Fibrillation Among Patients Hospitalized With Acute Myocardial Infarction: A Retrospective Case-Control Study.Reviews in cardiovascular medicine · 2025Article
- Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025Review
- Exploring the memory of the extracellular matrix using MASH-derived decellularized scaffolds.Journal of tissue engineeringArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Cardiovascular diseases (CVD) are one of the leading causes of death worldwide. From a modern point of view, endothelial dysfunction is considered as a key factor leading to the development of CVD. However, scientists have suggested that the main causes of the development of CVD might be functional disorders and phenotypic modulation of smooth muscle cells (SMCs) that make up the vascular wall. In this regard, the aim of our study was to evaluate the functional features of SMCs isolated from the tunica intima and from the tunica media of the thoracic part of the human aorta in patients with CVD. In our research we showed that phenotypic switching can occur in SMCs isolated from patients with aneurysms (n = 6), resulting in remodeling of the extracellular matrix and impaired interaction between cellular receptors. In addition, it is probable that the activation of complement-mediated phagocytosis as a result of LDL internalization by SMCs might be one of the key mechanisms in the process of aneurysm development.
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What Socratic 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 Socratic graph.