PMID- 31393254
OWN - NLM
STAT- MEDLINE
DCOM- 20210218
LR  - 20211102
IS  - 1875-6557 (Electronic)
IS  - 1573-403X (Print)
IS  - 1573-403X (Linking)
VI  - 16
IP  - 4
DP  - 2020
TI  - Endothelial to Mesenchymal Transition in the Cardiogenesis and Cardiovascular 
      Diseases.
PG  - 306-314
LID - 10.2174/1573403X15666190808100336 [doi]
AB  - Today, cardiovascular diseases remain a leading cause of morbidity and mortality 
      worldwide. Endothelial to mesenchymal transition (EndMT) does not only play a 
      major role in the course of development but also contributes to several 
      cardiovascular diseases in adulthood. EndMT is characterized by down-regulation 
      of the endothelial proteins and highly up-regulated fibrotic specific genes and 
      extracellular matrix-forming proteins. EndMT is also a transforming growth 
      factor- beta-driven (TGF-beta) process in which endothelial cells lose their 
      endothelial characteristics and acquire a mesenchymal phenotype with expression 
      of alpha-smooth muscle actin (alpha-SMA), fibroblastspecific protein 1, etc. EndMT is a 
      vital process during cardiac development, thus disrupted EndMT gives rise to the 
      congenital heart diseases, namely septal defects and valve abnormalities. In this 
      review, we have discussed the main signaling pathways and mechanisms 
      participating in the process of EndMT such as TGF-beta and Bone morphogenetic 
      protein (BMP), Wnt#, and Notch signaling pathway and also studied the role of 
      EndMT in physiological cardiovascular development and pathological conditions 
      including myocardial infarction, pulmonary arterial hypertension, congenital 
      heart defects, cardiac fibrosis, and atherosclerosis. As a perspective view, 
      having a clear understanding of involving cellular and molecular mechanisms in 
      EndMT and conducting Randomized controlled trials (RCTs) with a large number of 
      samples for involving pharmacological agents may guide us into novel therapeutic 
      approaches of congenital disorders and heart diseases.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Anbara, Taha
AU  - Anbara T
AD  - Department of Surgery, Erfan Specialty Hospital, Tehran, Iran.
FAU - Sharifi, Masuomeh
AU  - Sharifi M
AD  - Physiology Department, Faculty of Medicine, Iran University of Medical Sciences, 
      Tehran, Iran.
FAU - Aboutaleb, Nahid
AU  - Aboutaleb N
AD  - Physiology Research Center, Physiology Department, Faculty of Medicine, Iran 
      University of Medical Sciences, Tehran, Iran.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Cardiol Rev
JT  - Current cardiology reviews
JID - 101261935
SB  - IM
MH  - Cardiovascular Diseases/pathology/*physiopathology
MH  - Endothelial Cells/*metabolism
MH  - Heart Defects, Congenital/*physiopathology
MH  - Humans
PMC - PMC7903503
OTO - NOTNLM
OT  - Endothelial to mesenchymal transition
OT  - TGF-beta
OT  - cardiogenesis
OT  - cardiovascular disease
OT  - congenital heart diseases
EDAT- 2019/08/09 06:00
MHDA- 2021/02/20 06:00
PMCR- 2021/11/01
CRDT- 2019/08/09 06:00
PHST- 2019/04/28 00:00 [received]
PHST- 2019/07/05 00:00 [revised]
PHST- 2019/07/09 00:00 [accepted]
PHST- 2019/08/09 06:00 [pubmed]
PHST- 2021/02/20 06:00 [medline]
PHST- 2019/08/09 06:00 [entrez]
PHST- 2021/11/01 00:00 [pmc-release]
AID - CCR-EPUB-100200 [pii]
AID - CCR-16-306 [pii]
AID - 10.2174/1573403X15666190808100336 [doi]
PST - ppublish
SO  - Curr Cardiol Rev. 2020;16(4):306-314. doi: 10.2174/1573403X15666190808100336.