CCDC92 deficiency ameliorates podocyte lipotoxicity in diabetic kidney disease.

CCDC92 Diabetic kidney disease Lipotoxicity Podocytes

Journal

Metabolism: clinical and experimental
ISSN: 1532-8600
Titre abrégé: Metabolism
Pays: United States
ID NLM: 0375267

Informations de publication

Date de publication:
Jan 2024
Historique:
received: 10 08 2023
revised: 17 10 2023
accepted: 03 11 2023
pubmed: 13 11 2023
medline: 13 11 2023
entrez: 12 11 2023
Statut: ppublish

Résumé

Podocyte injury is considered as the most important early event contributing to diabetic kidney disease (DKD). Recent findings provide new insights into the roles of lipids and lipid-modulating proteins as key determinants of podocyte function in health and kidney disease. CCDC92, a novel member of coiled-coil domain-containing protein family, was indicated relevant to lipid metabolism, coronary heart disease and type 2 diabetes. However, the expression pattern and role of CCDC92 in the kidney is not clear. This study was designed to elucidate the contribution of CCDC92 in the pathogenesis of DKD. Sections with a pathological diagnosis of different classes of DKD, including subjects with mild DKD (class II, n = 6), subjects with moderate DKD (class III, n = 6) or subjects with severe DKD (class IV, n = 6), and control samples (n = 12) were detected for the expression level of CCDC92 and lipid accumulation. Two types of diabetic mice model (db/db and HFD/STZ) in podocyte-specific Ccdc92 knockout background were generated to clarify the role of CCDC92 in podocyte lipotoxicity. The level of CCDC92 was increased in renal biopsies sections from patients with DKD, which was correlated with eGFR and lipid accumulation in glomeruli. In animal studies, CCDC92 were also induced in the kidney from two independent diabetic models, especially in podocytes. Podocyte-specific deletion of Ccdc92 ameliorated podocyte injury and ectopic lipid deposition under diabetic condition. Mechanically, CCDC92 promoted podocyte lipotoxicity, at least in part through ABCA1 signaling-mediated lipid homeostasis. Our studies demonstrates that CCDC92 acts as a novel regulator of lipid homeostasis to promote podocyte injury in DKD, suggesting that CCDC92 might be a potential biomarker of podocyte injury in DKD, and targeting CCDC92 may be an effective innovative therapeutic strategy for patients with DKD.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
Podocyte injury is considered as the most important early event contributing to diabetic kidney disease (DKD). Recent findings provide new insights into the roles of lipids and lipid-modulating proteins as key determinants of podocyte function in health and kidney disease. CCDC92, a novel member of coiled-coil domain-containing protein family, was indicated relevant to lipid metabolism, coronary heart disease and type 2 diabetes. However, the expression pattern and role of CCDC92 in the kidney is not clear. This study was designed to elucidate the contribution of CCDC92 in the pathogenesis of DKD.
METHODS METHODS
Sections with a pathological diagnosis of different classes of DKD, including subjects with mild DKD (class II, n = 6), subjects with moderate DKD (class III, n = 6) or subjects with severe DKD (class IV, n = 6), and control samples (n = 12) were detected for the expression level of CCDC92 and lipid accumulation. Two types of diabetic mice model (db/db and HFD/STZ) in podocyte-specific Ccdc92 knockout background were generated to clarify the role of CCDC92 in podocyte lipotoxicity.
RESULTS RESULTS
The level of CCDC92 was increased in renal biopsies sections from patients with DKD, which was correlated with eGFR and lipid accumulation in glomeruli. In animal studies, CCDC92 were also induced in the kidney from two independent diabetic models, especially in podocytes. Podocyte-specific deletion of Ccdc92 ameliorated podocyte injury and ectopic lipid deposition under diabetic condition. Mechanically, CCDC92 promoted podocyte lipotoxicity, at least in part through ABCA1 signaling-mediated lipid homeostasis.
CONCLUSION CONCLUSIONS
Our studies demonstrates that CCDC92 acts as a novel regulator of lipid homeostasis to promote podocyte injury in DKD, suggesting that CCDC92 might be a potential biomarker of podocyte injury in DKD, and targeting CCDC92 may be an effective innovative therapeutic strategy for patients with DKD.

Identifiants

pubmed: 37952690
pii: S0026-0495(23)00328-1
doi: 10.1016/j.metabol.2023.155724
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

155724

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest All the authors declared no competing interests.

Auteurs

Fuwen Zuo (F)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Youzhao Wang (Y)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Xinlei Xu (X)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Ruihao Ding (R)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Wei Tang (W)

Department of Pathogenic Biology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Yu Sun (Y)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Xiaojie Wang (X)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Yan Zhang (Y)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Jichao Wu (J)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Yusheng Xie (Y)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.

Min Liu (M)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China. Electronic address: liuweimin@sdu.edu.cn.

Ziying Wang (Z)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China. Electronic address: wangziying@sdu.edu.cn.

Fan Yi (F)

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China; National Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan 250012, China. Electronic address: fanyi@sdu.edu.cn.

Classifications MeSH