The mechanism of TGF-β/miR-155/c-Ski regulates endothelial–mesenchymal transition in human coronary artery endothelial cells

J Wang, W He, X Xu, L Guo, Y Zhang, S Han… - Bioscience …, 2017 - portlandpress.com
Human coronary artery endothelial cells (HCAECs) have the potential to undergo fibrogenic
endothelial–mesenchymal transition (EndMT), which results in matrix-producing fibroblasts …

The Role of c‐SKI in Regulation of TGFβ‐Induced Human Cardiac Fibroblast Proliferation and ECM Protein Expression

J Wang, L Guo, D Shen, X Xu, J Wang… - Journal of Cellular …, 2017 - Wiley Online Library
Cardiac fibrosis is characterized by over‐deposition of extracellular matrix (ECM) proteins
and over‐proliferation of cardiac fibroblast, and contributes to both systolic and diastolic …

MiR-34a/miR-93 target c-Ski to modulate the proliferaton of rat cardiac fibroblasts and extracellular matrix deposition in vivo and in vitro

C Zhang, Y Zhang, H Zhu, J Hu, Z Xie - Cellular signalling, 2018 - Elsevier
Cardiac fibrosis is associated with diverse heart diseases. In response to different
pathological irritants, cardiac fibroblasts may be induced to proliferate and differentiate into …

[HTML][HTML] miRNA‑92a inhibits vascular smooth muscle cell phenotypic modulation and may help prevent in‑stent restenosis

F Jiang, B Zhang, X Zhang… - Molecular …, 2023 - spandidos-publications.com
The modulation of vascular smooth muscle cell (VSMC) phenotype during cellular
proliferation and migration may represent a potential therapeutic approach for vascular …

TGFβ triggers miR-143/145 transfer from smooth muscle cells to endothelial cells, thereby modulating vessel stabilization

M Climent, M Quintavalle, M Miragoli, J Chen… - Circulation …, 2015 - Am Heart Assoc
Rationale: The miR-143/145 cluster is highly expressed in smooth muscle cells (SMCs),
where it regulates phenotypic switch and vascular homeostasis. Whether it plays a role in …

MiR-200a modulates TGF-β1-induced endothelial-to-mesenchymal shift via suppression of GRB2 in HAECs

H Zhang, J Hu, L Liu - Biomedicine & Pharmacotherapy, 2017 - Elsevier
Endothelial-mesenchymal transition (EndMT) is closely associated with embryogenesis,
injury restitution, tissue neogenesis, tumor progressions and viscera fibrosis. EndMT may …

The role of miR-328 in high glucose-induced endothelial-to-mesenchymal transition in human umbilical vein endothelial cells

Y Chen, Q Yang, Y Zhan, J Ke, P Lv, J Huang - Life sciences, 2018 - Elsevier
Aims Endothelial-to-mesenchymal transition (EndMT) contribute to diabetic cardiac fibrosis,
the underlying mechanisms are poorly understood. In the study, we aimed to investigate the …

MiR‐154 directly suppresses DKK2 to activate Wnt signaling pathway and enhance activation of cardiac fibroblasts

LY Sun, ZD Bie, CH Zhang, H Li, LD Li… - Cell Biology …, 2016 - Wiley Online Library
Excessive proliferation of cardiac fibroblasts (CFs) and their transdifferentiation into
myofibroblasts leads to expression of α‐smooth muscle actin (α‐SMA), as well as excessive …

[HTML][HTML] Cardiomyocyte derived miR-328 promotes cardiac fibrosis by paracrinely regulating adjacent fibroblasts

D Zhao, C Li, H Yan, T Li, M Qian, N Zheng… - Cellular Physiology and …, 2018 - karger.com
Background/Aims: In our previous study, we demonstrated that elevated expression of miR-
328 is a potent determinant of cardiac fibrosis during myocardial infarction (MI). In the …

[PDF][PDF] MiR-154 promotes myocardial fibrosis through β-catenin signaling pathway.

P Dong, WJ Liu, ZH Wang - European Review for Medical & …, 2018 - europeanreview.org
OBJECTIVE: To discover the mechanisms of miR-154 affecting myocardial fibrosis.
PATIENTS AND METHODS: Human cardiac fibroblasts (CFs) were cultured in medium …