Τίτλος:
FAK/Src family of kinases: Protective or aggravating factor for ischemia reperfusion injury in nervous system?
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Introduction: The focal adhesion kinase (FAK) and the Src families of kinases are subfamilies of the non-receptor protein tyrosine kinases. FAK activity is regulated by gene amplification, alternative splicing and phosporylation/dephosphorylation. FAK/Src complex has been found to participate through various pathways in neuronal models of ischemia-reperfusion injury (IRI) with conflicting results. The aim of the present review is to summarize the currently available data on this subject. Areas covered: The MEDLINE/PubMed database was searched for publications with the medical subject heading IRI and FAK and/or Src, nervous system. We restricted our search till 2014. We identified 93 articles that were available in English as abstracts or/and full-text articles that were deemed appropriate for our review. Expert opinion: FAK has been found to have a beneficial preconditioning effect on IRI through activation via the protein kinase C (PKC) pathway by anesthetic agents. Of great importance are the interactions between FAK/Src and VEGF that has been already detected as a protective mean for IRI. The effect of VEGF administration might depend on dose as well as on time of administration. A Ca2+/calmodulin-dependent protein kinase II or PKC inhibitors seem to have protective effects on IRI by inhibiting ion channels activation. © 2014 Informa UK, Ltd. All rights reserved.
Συγγραφείς:
Bikis, C.
Moris, D.
Vasileiou, I.
Patsouris, E.
Theocharis, S.
Περιοδικό:
Expert Opinion on Therapeutic Targets
Εκδότης:
Informa Healthcare
Λέξεις-κλειδιά:
anesthetic agent; calcium calmodulin dependent protein kinase II; focal adhesion kinase; protein kinase C inhibitor; protein kinase p60; vasculotropin; anesthetic agent; focal adhesion kinase; protein kinase C; protein tyrosine kinase; vasculotropin A, enzyme activation; enzyme phosphorylation; human; Medical Subject Headings; Medline; nervous system injury; reperfusion injury; Review; animal; antagonists and inhibitors; ischemic preconditioning; metabolism; neurologic disease; pathophysiology; phosphorylation; reperfusion injury, Anesthetics; Animals; Focal Adhesion Protein-Tyrosine Kinases; Humans; Ischemic Preconditioning; Nervous System Diseases; Phosphorylation; Protein Kinase C; Reperfusion Injury; src-Family Kinases; Vascular Endothelial Growth Factor A
DOI:
10.1517/14728222.2014.990374
