Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0606920200280030213
Biomolecules & Therapeutics
2020 Volume.28 No. 3 p.213 ~ p.221
Fyn Kinase: A Potential Therapeutic Target in Acute Kidney Injury
Uddin Md Jamal

Dorotea Debra
Pak Eun-Seon
Ha Hun-Joo
Abstract
Acute kidney injury (AKI) is a common disease with a complex pathophysiology which significantly contributes to the development of chronic kidney disease and end stage kidney failure. Preventing AKI can consequently reduce mortality, morbidity, and healthcare burden. However, there are no effective drugs in use for either prevention or treatment of AKI. Developing therapeutic agents with pleiotropic effects covering multiple pathophysiological pathways are likely to be more effective in attenuating AKI. Fyn, a nonreceptor tyrosine kinase, has been acknowledged to integrate multiple injurious stimuli in the kidney. Limited studies have shown increased Fyn transcription level and activation under experimental AKI. Activated Fyn kinase propagates various downstream signaling pathways associated to the progression of AKI, such as oxidative stress, inflammation, endoplasmic reticulum stress, as well as autophagy dysfunction. The versatility of Fyn kinase in mediating various pathophysiological pathways suggests that its inhibition can be a potential strategy in attenuating AKI.
KEYWORD
Fyn kinase, Acute kidney injury, Inflammation, Oxidative stress, ER stress, Autophagy
FullTexts / Linksout information
 
Listed journal information
SCI(E) ÇмúÁøÈïÀç´Ü(KCI) KoreaMed