ArticleJournal of cellular and molecular medicine2020
MFGE8 is down-regulated in cardiac fibrosis and attenuates endothelial-mesenchymal transition through Smad2/3-Snail signalling pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- Proteomic pathways across the ejection fraction spectrum in patients with heart failure and diabetes mellitus: an EXSCEL trial substudy.Scientific reports · 2025Trial
- FGFR1/KLB-MFG-E8 Maintains Microvascular Integrity and Adaptive Cardiac Remodeling.Circulation research · 2026Article
- SNAI2/SLUG: a key regulator of endothelial-to-mesenchymal transition and vascular remodeling in cardiovascular diseases.Journal of cardiothoracic surgery · 2026Review
- Endothelial Cell-Related Proteins in Plasma Predict Major Adverse Cardiovascular Events and Worsening Heart Failure in Patients With Hypertrophic Cardiomyopathy.Journal of the American Heart Association · 2025Article
- Deciphering the role of MFGE8 in lactation using CRISPR-CAS9 based gene editing in Buffalo mammary epithelial cells.Scientific reports · 2025Article
- Transferrin receptor knockdown attenuates atrial fibrillation by inhibiting cardiomyocyte ferroptosis and atrial fibrosis.Experimental animals · 2025Article
- Endothelial-Mesenchymal Transition and Possible Role of Cytokines in Streptozotocin-Induced Diabetic Heart.Biomedicines · 2025Article
- Molecular mechanisms of endothelial-mesenchymal transition and its pathophysiological feature in cerebrovascular disease.Cell & bioscience · 2025Review
- MFGE8 regulates the EndoMT of HLMECs through the BMP signaling pathway and fibrosis in acute lung injury.Respiratory research · 2025Article
- MFG-E8 in Kawasaki Disease: Role in Endothelial Injury and Diagnostic Potential.Journal of inflammation research · 2025Article
- The novel anthraquinone compound Kanglexin prevents endothelial-to-mesenchymal transition in atherosclerosis by activating FGFR1 and suppressing integrin β1/TGFβ signaling.Frontiers of medicine · 2024Article
- Generation and characterisation of scalable and stable human pluripotent stem cell-derived microvascular-like endothelial cells for cardiac applications.Angiogenesis · 2024Article
- Article
- Epidermal Growth Factor-Like Repeats and Discoidin I-Like Domains 3 Deficiency Attenuates Dilated Cardiomyopathy by Inhibiting Ubiquitin Specific Peptidase 10 Dependent Smad4 Deubiquitination.Journal of the American Heart Association · 2024Article
- Triptolide attenuates cardiac remodeling by inhibiting pyroptosis and EndMT via modulating USP14/Keap1/Nrf2 pathway.Heliyon · 2024Article
- Zhilong Huoxue Tongyu capsule alleviates myocardial fibrosis by improving endothelial cell dysfunction.Journal of traditional and complementary medicine · 2024Article
- Mitochondrial reactive oxygen species impact human fibroblast responses to protracted γ-ray exposures.International journal of radiation biology · 2024Article
- Experimental Models to Study Endothelial to Mesenchymal Transition in Myocardial Fibrosis and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Fibroblasts generate topographical cues that steer cancer cell migration.Science advances · 2023Article
- CCR2 macrophage response determines the functional outcome following cardiomyocyte transplantation.Genome medicine · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial-mesenchymal transition (EndMT) is a major source of transformed cardiac fibroblasts, which is reported to play a key role in cardiac fibrosis (CF), a pathogenesis of cardiovascular diseases such as heart failure, myocardial infarction and atrial fibrillation. Nonetheless, the specific mechanism underlying the progression of EndMT to CF is still largely unknown. In this study, we aimed to investigate the role of milk fat globule-EGF factor 8 (MFGE8), a kind of soluble glycoprotein, in TGF-β1-induced EndMT. In animal experiments, the expression of MFGE8 was found down-regulated in the left ventricle and aorta of rats after transverse aortic constriction (TAC) compared with the sham group, especially in endothelial cells (ECs). In in vitro cultured ECs, silencing MFGE8 with small interfering RNA (siRNA) was found to promote the process of TGF-β1-induced EndMT, whereas administration of recombinant human MFGE8 (rh-MFGE8) attenuated the process. Moreover, activated Smad2/3 signalling pathway after TGF-β1 treatment and EndMT-related transcription factors, such as Snail, Twist and Slug, was potentiated by MFGE8 knock-down but inhibited by rh-MFGE8. In conclusion, our experiments indicate that MFGE8 might play a protective role in TGF-β1-induced EndMT and might be a potential therapeutic target for cardiac fibrosis.
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