Evidence map›Paper›PMID 42457923›Full record

ArticleCell death and differentiation2026

ZDHHC8-mediated S-palmitoylation of RAD21 causes mitochondrial dysfunction in diabetic nephropathy via inhibiting ACSM3 transcription.

Wei Chen, Yinyin Chen, Shaobin Duan, Hao Li, Yang Gao, Weiying Zhang, Guoyong Liu, Jiayi Wang, Xiaofei Peng, Liyu He

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Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Wei Chen *Department of Nephrology, The Second Xiangya Hospital, Central South University, Key Lab of Kidney Disease and Blood Purification in Hunan, Changsha, PR China.
Yinyin Chen *Department of Nephrology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Hunan Clinical Research Center for Chronic Kidney Disease, Changsha, PR China.
Shaobin DuanDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Key Lab of Kidney Disease and Blood Purification in Hunan, Changsha, PR China.
Hao LiDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Key Lab of Kidney Disease and Blood Purification in Hunan, Changsha, PR China.
Yang GaoDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Key Lab of Kidney Disease and Blood Purification in Hunan, Changsha, PR China.
Weiying ZhangDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Key Lab of Kidney Disease and Blood Purification in Hunan, Changsha, PR China.
Guoyong LiuDepartment of Nephrology, The First Affiliated Hospital of Changde Vocational Technical College, Changde, PR China.
Jiayi WangDepartment of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, PR China.
Xiaofei PengDepartment of Rheumatology and Immunology, The Second Xiangya Hospital, Central South University, Changsha, PR China.
Liyu HeDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Key Lab of Kidney Disease and Blood Purification in Hunan, Changsha, PR China. heliyu1124@csu.edu.cn.ORCID http://orcid.org/0000-0002-6759-2069

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubulointerstitial injury exerts a key role in diabetic nephropathy (DN) development; however, its potential mechanism is still unclear. We explored the role and molecular mechanisms of RAD21 cohesin complex component (RAD21) in mitochondrial dysfunction during tubulointerstitial injury of DN. We found that RAD21 was down-regulated, but its S-palmitoylation level was up-regulated in DN. RAD21 overexpression attenuated renal tubulointerstitial injury, fibrosis and mitochondrial dysfunction in DN. In addition, zinc finger DHHC-type palmitoyltransferase8 (ZDHHC8) served as a key acetyltransferase that catalyzed RAD21 S-palmitoylation at C78 site, which led to heat shock protein member 8 (HSPA8)-mediated lysosomal degradation of RAD21. Down-regulation of RAD21 repressed the transcription and expression of ACSM3. ACSM3 deficiency abrogated the beneficial effect of RAD21 overexpression on mitochondrial dysfunction during tubulointerstitial injury in DN. In conclusion, ZDHHC8-mediated S-palmitoylation of RAD21 favored its lysosomal degradation with assistance of HSPA8, which repressed ACSM3 transcription to cause mitochondrial dysfunction, thereby accelerating DN progression.

Identifiers

PMID42457923

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.