Regulation of autophagy in leukocytes through RNA N6-adenosine methylation in chronic kidney disease patients

Chao Yung Wang*, Tien An Lin, Ming Yun Ho, Jih Kai Yeh, Ming Lung Tsai, Kuo Chun Hung, I. Chang Hsieh, Ming Shien Wen

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

12 Scopus citations


Patients with chronic kidney diseases have multiple cellular dysfunctions leading to increased atherosclerosis, impaired immunity, and disturbed metabolism. However, it is unclear what is the fundamental signaling served as a marker or as a mediator for the dysregulated function in their leukocytes or tissues. Here we hypothesized that the N6-Methyladenosine (m6A) modification of the RNA in the leukocytes is responsible for the cellular dysfunction in chronic kidney diseases. Patients with chronic kidney diseases had significantly less m6A abundances in leukocytes and elevated RNA demethylase FTO proteins. The uremic toxin, indoxyl sulfate, activated the autophagy flux through modulation of FTO and m6A modifications in RNA. Notably, knockdown of FTO or inhibit the m6A by 3-deazaadenosine blocks the effects of indoxyl sulfate on autophagy activation in cells. These findings provide new insights into the mechanisms underlying chronic kidney disease-associated cellular dysfunction. Targeting RNA m6A modification may be a novel strategy for the treatment of chronic kidney diseases and autophagy.

Original languageEnglish
Pages (from-to)953-959
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - 05 07 2020

Bibliographical note

Publisher Copyright:
© 2020 Elsevier Inc.


  • Autophagy
  • CKD
  • Leukocytes
  • RNA demethylase
  • Uremia


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