The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis

Abstract Acute kidney injury (AKI) is a serious clinical condition whose underlying mechanisms remain unclear. Here we identify a long non-coding RNA, RSDR, as a critical regulator of renal protection in AKI. RSDR interacts with the RNA-binding protein hnRNPK, forming a positive feedback loop that e...

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Main Authors: Bojun Li, Fangyou Lin, Baofeng Song, ShangTing Han, Zehua Ye, Yushi Sun, Peihan Wang, Yuqi Xia, Weimin Yu, Xiangjun Zhou, Fan Cheng
Format: Article
Language:English
Published: Nature Portfolio 2025-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-62433-2
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author Bojun Li
Fangyou Lin
Baofeng Song
ShangTing Han
Zehua Ye
Yushi Sun
Peihan Wang
Yuqi Xia
Weimin Yu
Xiangjun Zhou
Fan Cheng
author_facet Bojun Li
Fangyou Lin
Baofeng Song
ShangTing Han
Zehua Ye
Yushi Sun
Peihan Wang
Yuqi Xia
Weimin Yu
Xiangjun Zhou
Fan Cheng
author_sort Bojun Li
collection DOAJ
description Abstract Acute kidney injury (AKI) is a serious clinical condition whose underlying mechanisms remain unclear. Here we identify a long non-coding RNA, RSDR, as a critical regulator of renal protection in AKI. RSDR interacts with the RNA-binding protein hnRNPK, forming a positive feedback loop that enhances the transcription of DHODH, a key ferroptosis-suppressing gene. Mechanistically, RSDR promotes the nuclear retention of hnRNPK and facilitates epigenetic activation of DHODH, thereby limiting ferroptosis in renal tubular epithelial cells. In vivo overexpression of RSDR attenuates ferroptosis and preserves renal function in male mice during AKI. Clinically, urinary RSDR levels are significantly reduced in patients with AKI, and machine learning analysis suggests potential utility in disease detection. These findings highlight RSDR as a central regulator of ferroptosis and provide mechanistic insights into lncRNA-mediated tubular protection in AKI.
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institution Kabale University
issn 2041-1723
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publishDate 2025-08-01
publisher Nature Portfolio
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series Nature Communications
spelling doaj-art-bbe58b2de9104e4da8df2684d6dee8252025-08-20T03:43:10ZengNature PortfolioNature Communications2041-17232025-08-0116112010.1038/s41467-025-62433-2The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosisBojun Li0Fangyou Lin1Baofeng Song2ShangTing Han3Zehua Ye4Yushi Sun5Peihan Wang6Yuqi Xia7Weimin Yu8Xiangjun Zhou9Fan Cheng10Department of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityAbstract Acute kidney injury (AKI) is a serious clinical condition whose underlying mechanisms remain unclear. Here we identify a long non-coding RNA, RSDR, as a critical regulator of renal protection in AKI. RSDR interacts with the RNA-binding protein hnRNPK, forming a positive feedback loop that enhances the transcription of DHODH, a key ferroptosis-suppressing gene. Mechanistically, RSDR promotes the nuclear retention of hnRNPK and facilitates epigenetic activation of DHODH, thereby limiting ferroptosis in renal tubular epithelial cells. In vivo overexpression of RSDR attenuates ferroptosis and preserves renal function in male mice during AKI. Clinically, urinary RSDR levels are significantly reduced in patients with AKI, and machine learning analysis suggests potential utility in disease detection. These findings highlight RSDR as a central regulator of ferroptosis and provide mechanistic insights into lncRNA-mediated tubular protection in AKI.https://doi.org/10.1038/s41467-025-62433-2
spellingShingle Bojun Li
Fangyou Lin
Baofeng Song
ShangTing Han
Zehua Ye
Yushi Sun
Peihan Wang
Yuqi Xia
Weimin Yu
Xiangjun Zhou
Fan Cheng
The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis
Nature Communications
title The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis
title_full The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis
title_fullStr The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis
title_full_unstemmed The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis
title_short The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis
title_sort long non coding rna rsdr protects against acute kidney injury in mice by interacting with hnrnpk to regulate dhodh mediated ferroptosis
url https://doi.org/10.1038/s41467-025-62433-2
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