Dysregulation of Calcium Homeostasis: An Important Factor Leading to Ferroptosis in Cardiovascular Diseases.

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Biology International Pub Date : 2025-03-05 DOI:10.1002/cbin.70012

Yifan Zhang, Leiyin Zheng, Tongtong Che, Ning Meng

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Abstract

Cardiovascular disease is a circulatory system disease involving the heart and blood vessels, which is one of the main causes of human health loss and even life-threatening. Ca²⁺ is an important signal molecule. Free calcium ions in the cytoplasm are involved in various physiological and biochemical reactions of cells. Ferroptosis is a programmed cell death driven by lipid peroxidation dependent on free ferrous ions. The essence of ferroptosis is the accumulation of lipid peroxide caused by the increase of intracellular ferrous ion content, which leads to the damage of the phospholipid membrane and eventually cell death. Studies have shown that calcium homeostasis and ferroptosis are involved in the occurrence and development of cardiovascular diseases, but the relationship between them remains to be clarified. This article reviews the various pathways regulating calcium homeostasis in cells and the occurrence and development mechanism of ferroptosis, and discusses the relationship between the two in cardiovascular diseases, which is expected to provide novel and important strategies for alleviating and treating cardiovascular diseases.

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钙稳态失调：心血管疾病中导致铁下沉的重要因素。

心血管疾病是一种累及心脏和血管的循环系统疾病，是造成人类健康损失甚至危及生命的主要原因之一。Ca2+是一种重要的信号分子。细胞质中的游离钙离子参与细胞的各种生理生化反应。铁下垂是一种程序性细胞死亡驱动的脂质过氧化依赖于自由铁离子。铁沉的实质是细胞内铁离子含量增加引起的脂质过氧化积累，导致磷脂膜损伤，最终导致细胞死亡。研究表明钙稳态和铁下垂参与心血管疾病的发生发展，但两者之间的关系尚不清楚。本文综述了细胞内钙稳态的各种调节途径和铁下沉的发生发展机制，并探讨了两者在心血管疾病中的关系，以期为心血管疾病的缓解和治疗提供新的重要策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Biology International 生物-细胞生物学

CiteScore

7.60

自引率

0.00%

发文量

208

审稿时长

1 months

期刊介绍： Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.