Fyn kinase: A potential therapeutic target in acute kidney injury

Md Jamal Uddin, Debra Dorotea, Eun Seon Pak, Hunjoo Ha

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


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 health-care 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 non-receptor 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.

Original languageEnglish
Pages (from-to)213-221
Number of pages9
JournalBiomolecules and Therapeutics
Issue number3
StatePublished - 2020

Bibliographical note

Funding Information:
This work was supported by a National Research Foundation grant (No. 2017R1D1A1B03028835) and Korean Health Technology R&D project through Korea Health Industry Development Institute (No. HI18C0695), Republic of Korea. Dr. Md Jamal Uddin is supported by the Korean Research Fellowship Program (No. 2015H1D3A1062189) and RP-Grant 2020 of Ewha Womans University, Republic of Korea.

Publisher Copyright:
© 2020 The Korean Society of Applied Pharmacology.


  • Acute kidney injury
  • Autophagy
  • ER stress
  • Fyn kinase
  • Inflammation
  • Oxidative stress


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