TY - JOUR
T1 - Acute lung injury
T2 - The therapeutic role of Rho kinase inhibitors
AU - Abedi, Farshad
AU - Hayes, A. Wallace
AU - Reiter, Russel
AU - Karimi, Gholamreza
N1 - Funding Information:
The authors are thankful to Mashhad University of Medical Sciences, Iran.
Publisher Copyright:
© 2020 Elsevier Ltd
PY - 2020/5
Y1 - 2020/5
N2 - Acute lung injury (ALI) is a pulmonary illness with high rates of mortality and morbidity. Rho GTPase and its downstream effector, Rho kinase (ROCK), have been demonstrated to be involved in cell adhesion, motility, and contraction which can play a role in ALI. The electronic databases of Google Scholar, Scopus, PubMed, and Web of Science were searched to obtain relevant studies regarding the role of the Rho/ROCK signaling pathway in the pathophysiology of ALI and the effects of specific Rho kinase inhibitors in prevention and treatment of ALI. Upregulation of the RhoA/ROCK signaling pathway causes an increase of inflammation, immune cell migration, apoptosis, coagulation, contraction, and cell adhesion in pulmonary endothelial cells. These effects are involved in endothelium barrier dysfunction and edema, hallmarks of ALI. These effects were significantly reversed by Rho kinase inhibitors. Rho kinase inhibition offers a promising approach in ALI [ARDS] treatment.
AB - Acute lung injury (ALI) is a pulmonary illness with high rates of mortality and morbidity. Rho GTPase and its downstream effector, Rho kinase (ROCK), have been demonstrated to be involved in cell adhesion, motility, and contraction which can play a role in ALI. The electronic databases of Google Scholar, Scopus, PubMed, and Web of Science were searched to obtain relevant studies regarding the role of the Rho/ROCK signaling pathway in the pathophysiology of ALI and the effects of specific Rho kinase inhibitors in prevention and treatment of ALI. Upregulation of the RhoA/ROCK signaling pathway causes an increase of inflammation, immune cell migration, apoptosis, coagulation, contraction, and cell adhesion in pulmonary endothelial cells. These effects are involved in endothelium barrier dysfunction and edema, hallmarks of ALI. These effects were significantly reversed by Rho kinase inhibitors. Rho kinase inhibition offers a promising approach in ALI [ARDS] treatment.
KW - Acute lung injury
KW - Endothelial cell
KW - Fasudil
KW - Fasudil (PubChem CID: 3547)
KW - Netarsudil (PubChem CID: 66599893)
KW - Oleic acid (PubChem CID: 445639)
KW - Paraquat (PubChem CID: 15939)
KW - ROCK
KW - Rho kinase inhibitor
KW - Ripasudil (PubChem CID: 9863672)
KW - Simvastatin (PubChem CID: 54454)
KW - Y-27632 (PubChem CID: 9901617)
UR - http://www.scopus.com/inward/record.url?scp=85081009038&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85081009038&partnerID=8YFLogxK
U2 - 10.1016/j.phrs.2020.104736
DO - 10.1016/j.phrs.2020.104736
M3 - Review article
C2 - 32135249
AN - SCOPUS:85081009038
SN - 1043-6618
VL - 155
JO - Pharmacological Research
JF - Pharmacological Research
M1 - 104736
ER -