Ferroptosis: an important player in the inflammatory response in diabetic nephropathy.

diabetic nephropathy ferroptosis inflammation oxidative stress signaling pathway

Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2023
Historique:
received: 14 09 2023
accepted: 15 11 2023
medline: 19 12 2023
pubmed: 19 12 2023
entrez: 19 12 2023
Statut: epublish

Résumé

Diabetic nephropathy (DN) is a chronic inflammatory disease that affects millions of diabetic patients worldwide. The key to treating of DN is early diagnosis and prevention. Once the patient enters the clinical proteinuria stage, renal damage is difficult to reverse. Therefore, developing early treatment methods is critical. DN pathogenesis results from various factors, among which the immune response and inflammation play major roles. Ferroptosis is a newly discovered type of programmed cell death characterized by iron-dependent lipid peroxidation and excessive ROS production. Recent studies have demonstrated that inflammation activation is closely related to the occurrence and development of ferroptosis. Moreover, hyperglycemia induces iron overload, lipid peroxidation, oxidative stress, inflammation, and renal fibrosis, all of which are related to DN pathogenesis, indicating that ferroptosis plays a key role in the development of DN. Therefore, this review focuses on the regulatory mechanisms of ferroptosis, and the mutual regulatory processes involved in the occurrence and development of DN and inflammation. By discussing and analyzing the relationship between ferroptosis and inflammation in the occurrence and development of DN, we can deepen our understanding of DN pathogenesis and develop new therapeutics targeting ferroptosis or inflammation-related regulatory mechanisms for patients with DN.

Identifiants

pubmed: 38111578
doi: 10.3389/fimmu.2023.1294317
pmc: PMC10725962
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

1294317

Informations de copyright

Copyright © 2023 Li, Li, Zhang, Chen, Shu, Yang, Chu and Liu.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Jialing Li (J)

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.

Luxin Li (L)

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.
Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, China.

Zhen Zhang (Z)

Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, China.
School of First Clinical Medical College, Mudanjiang Medical University, Mudanjiang, China.

Peijian Chen (P)

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.
Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, China.

Haiying Shu (H)

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.

Can Yang (C)

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.

Yanhui Chu (Y)

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.
Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, China.

Jieting Liu (J)

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.
Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, China.

Classifications MeSH