ArticleLipids in health and disease2021
Negative correlation between endoglin levels and coronary atherosclerosis.
Article in Lipids in health and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Elucidating the role of SF3B3 in coronary atherosclerosis: integrating bioinformatics and machine learning for advanced insights.Journal of cardiothoracic surgery · 2026Article
- Elucidating the role of LGALS3BP in coronary atherosclerosis: integrating bioinformatics and machine learning for advanced insights.Journal of cardiothoracic surgery · 2025Article
- Elucidating the role of KLRD1 in coronary atherosclerosis: harnessing bioinformatics and machine learning to advance understanding.Journal of cardiothoracic surgery · 2025Article
- LncRNA uc003pxg.1 Interacts With miR-339-5p Promote Vascular Endothelial Cell Proliferation, Migration and Angiogenesis.Korean circulation journal · 2025Article
- Elucidating the role of KCTD10 in coronary atherosclerosis: Harnessing bioinformatics and machine learning to advance understanding.Scientific reports · 2025Article
- Integrative bioinformatics and machine learning approach unveils potential biomarkers linking coronary atherosclerosis and fatty acid metabolism-associated gene.Journal of cardiothoracic surgery · 2025Article
- Activins and Inhibins in Cardiovascular Pathophysiology.Biomolecules · 2024Review
- Exploration of the influence of GOLGA8B on prostate cancer progression and the resistance of castration-resistant prostate cancer to cabazitaxel.Discover oncology · 2024Article
- Unlocking potential biomarkers bridging coronary atherosclerosis and pyrimidine metabolism-associated genes through an integrated bioinformatics and machine learning approach.BMC cardiovascular disorders · 2024Article
- Low Plasma Levels of Soluble Endoglin and Cardiovascular Events in Patients Undergoing Coronary Angiography.Biomedicines · 2023Article
- Interaction between the expression of hsa_circRPRD1A and hsa_circHERPUD2 and classical coronary risk factors promotes the development of coronary artery disease.BMC medical genomics · 2023Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundCoronary artery disease (CAD) is a common cardiovascular disease, and abnormal blood lipid metabolism is an important risk factor. Transforming growth factor-ß (TGF-ß) and its receptor (TGF-ßR) can inhibit the release of inflammatory factors through the SMAD pathway-mediated immune response, thereby suppressing the progression of CAD. Endoglin (TGF-ßRIII), a TGF-ßR family homologous receptor protein, is directly involved in the immunoregulatory process, but the exact mechanism is unclear. This study aimed to clarify the pathophysiological effects of endoglin on the development of atherosclerosis and to explore the mechanism of the signalling pathway.
methodsWe downloaded the GEO dataset to perform a functional analysis of SMAD family activity and TGF-ß receptor protein expression in the monocyte expression profiles of patients with familial hyperlipidaemia (FH). The effect of endoglin on endothelial cell proliferation, migration, and apoptosis was examined by disrupting the endoglin gene in human umbilical vein endothelial cells (HUVECs) and validated by western blotting. The related genes and pathways regulated by endoglin were obtained by analysing the sequencing data.
resultsResearch has shown that interference with endoglin can promote the proliferation and migration and significantly inhibit the apoptosis of vascular endothelial cells. Interference with endoglin particularly encourages the expression of VEGFB in vascular endothelial cells.
conclusionThe endoglin gene in vascular endothelial cells regulates the PI3K-Akt, Wnt, TNF, and cellular metabolism pathways by activating the SMAD pathway. RAB26, MR1, CCL2, SLC29A4, IBTK, VEGFB, and GOLGA8B play critical roles. Endoglin interacts closely with 11 proteins such as CCL2 and SEPRINE1, which participate in the vital pathway of plaque formation. Interference with endoglin can alter the course of coronary atherosclerosis.
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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.