Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment
m6A modification has been reported to play roles in many developmental and pathological processes, but its role in AKI remains poorly understood. Here, the authors show the role and the mechanism of the m6A demethylase, ALKBH5 on IRI induced AKI.
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Format: | Article |
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Nature Portfolio
2023-03-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-023-36747-y |
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author | Juntao Chen Cuidi Xu Kun Yang Rifeng Gao Yirui Cao Lifei Liang Siyue Chen Shihao Xu Ruiming Rong Jina Wang Tongyu Zhu |
author_facet | Juntao Chen Cuidi Xu Kun Yang Rifeng Gao Yirui Cao Lifei Liang Siyue Chen Shihao Xu Ruiming Rong Jina Wang Tongyu Zhu |
author_sort | Juntao Chen |
collection | DOAJ |
description | m6A modification has been reported to play roles in many developmental and pathological processes, but its role in AKI remains poorly understood. Here, the authors show the role and the mechanism of the m6A demethylase, ALKBH5 on IRI induced AKI. |
first_indexed | 2024-04-09T22:47:16Z |
format | Article |
id | doaj.art-ac2ae51bb26446b2ad18b825295ea9ef |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-04-09T22:47:16Z |
publishDate | 2023-03-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
spelling | doaj.art-ac2ae51bb26446b2ad18b825295ea9ef2023-03-22T11:47:27ZengNature PortfolioNature Communications2041-17232023-03-0114111710.1038/s41467-023-36747-yInhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitmentJuntao Chen0Cuidi Xu1Kun Yang2Rifeng Gao3Yirui Cao4Lifei Liang5Siyue Chen6Shihao Xu7Ruiming Rong8Jina Wang9Tongyu Zhu10Department of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular DiseasesThe Fifth People’s Hospital of Shanghai, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan UniversityDepartment of Urology, Zhongshan Hospital, Fudan Universitym6A modification has been reported to play roles in many developmental and pathological processes, but its role in AKI remains poorly understood. Here, the authors show the role and the mechanism of the m6A demethylase, ALKBH5 on IRI induced AKI.https://doi.org/10.1038/s41467-023-36747-y |
spellingShingle | Juntao Chen Cuidi Xu Kun Yang Rifeng Gao Yirui Cao Lifei Liang Siyue Chen Shihao Xu Ruiming Rong Jina Wang Tongyu Zhu Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment Nature Communications |
title | Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment |
title_full | Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment |
title_fullStr | Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment |
title_full_unstemmed | Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment |
title_short | Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment |
title_sort | inhibition of alkbh5 attenuates i r induced renal injury in male mice by promoting ccl28 m6a modification and increasing treg recruitment |
url | https://doi.org/10.1038/s41467-023-36747-y |
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