國家衛生研究院 NHRI:Item 3990099045/12672
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    題名: Regulation of autophagy in leukocytes through RNA N6-adenosine methylation in chronic kidney disease patients
    作者: Wang, CY;Lin, TA;Ho, MY;Yeh, JK;Tsai, ML;Hung, KC;Hsieh, IC;Wen, MS
    貢獻者: Institute of Cellular and Systems Medicine
    摘要: 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.
    日期: 2020-07
    關聯: Biochemical and Biophysical Research Communications. 2020 Jul;527(4):953-959.
    Link to: http://dx.doi.org/10.1016/j.bbrc.2020.04.138
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0006-291X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000538861300017
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85084745950
    顯示於類別:[王朝永] 期刊論文

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