Ferroptosis in cardiac hypertrophy and heart failure.

Cardiac hypertrophy Ferroptosis Heart failure Inducer and inhibitor Regulation mechanism

Journal

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
ISSN: 1950-6007
Titre abrégé: Biomed Pharmacother
Pays: France
ID NLM: 8213295

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 08 08 2023
revised: 08 10 2023
accepted: 17 10 2023
medline: 15 11 2023
pubmed: 26 10 2023
entrez: 25 10 2023
Statut: ppublish

Résumé

Heart failure has become a public health problem that we cannot avoid choosing to face in today's context. In the case of heart failure, pathological cardiac hypertrophy plays a major role because of its condition of absolute increase in ventricular mass under various stresses. Ferroptosis, it could be defined as regulatory mechanisms that regulate cell death in the absence of apoptosis in iron-dependent cells. This paper introduces various new research findings on the use of different regulatory mechanisms of cellular ferroptosis for the treatment of heart failure and cardiac hypertrophy, providing new therapeutic targets and research directions for clinical treatment. The role and mechanism of ferroptosis in the field of heart failure has been increasingly demonstrated, and the relationship between cardiac hypertrophy, which is one of the causes of heart failure, is also an area of research that we should focus on. In addition, the latest applications and progress of inducers and inhibitors of ferroptosis are reported in this paper, updating the breakthroughs in their fields.

Identifiants

pubmed: 37879210
pii: S0753-3322(23)01563-9
doi: 10.1016/j.biopha.2023.115765
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

115765

Informations de copyright

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

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose.

Auteurs

Kuo Zhang (K)

Department of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, Shenyang 110122, China.

Xin-Miao Tian (XM)

Department of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, Shenyang 110122, China.

Wei Li (W)

Department of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, Shenyang 110122, China.

Li-Ying Hao (LY)

Department of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, Shenyang 110122, China. Electronic address: lyhao@cmu.edu.cn.

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Classifications MeSH