Iron Dysregulation in Cardiovascular Diseases

¹ Geriatric Diseases Institute of Chengdu, Center for Medicine Research and Translation, Chengdu Fifth People's Hospital, 611137 Chengdu, Sichuan, China

^*Correspondence: mqdong@cdutcm.edu.cn (Mingqing Dong)

Rev. Cardiovasc. Med. 2024, 25(1), 16; https://doi.org/10.31083/j.rcm2501016

Submitted: 7 August 2023 | Revised: 7 October 2023 | Accepted: 24 October 2023 | Published: 10 January 2024

This is an open access article under the CC BY 4.0 license.

Abstract

Iron metabolism plays a crucial role in various physiological functions of the human body, as it is essential for the growth and development of almost all organisms. Dysregulated iron metabolism—manifested either as iron deficiency or overload—is a significant risk factor for the development of cardiovascular disease (CVD). Moreover, emerging evidence suggests that ferroptosis, a form of iron-dependent programed cell death, may also contribute to CVD development. Understanding the regulatory mechanisms of iron metabolism and ferroptosis in CVD is important for improving disease management. By integrating different perspectives and expertise in the field of CVD-related iron metabolism, this overview provides insights into iron metabolism and CVD, along with approaches for diagnosing, treating, and preventing CVD associated with iron dysregulation.

Keywords

iron metabolism

homeostasis

cardiovascular disease

dysregulation

Highlights

Dysregulation of iron homeostasis, range from iron deficiency to iron-overload, contributes to the pathological process of CVDs.
Ferroptosis is a type of iron-dependent cell death and mainly driven by lipid peroxidation.
The ferroptosis is regulated by various metabolic processes, including iron, lipid and glutathione metabolism.
Ferroptosis could induce ROS, mitochondrial dysfunction and inflammation, that contribute to the pathological process of CVDs.
Keeping the homeostasis or targeting ferroptosis provides new therapeutic opportunities for CVDs.

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Funding

2023NSFSC0531/Natural Science Foundation of Sichuan Province

2022036/Chengdu Municipal Health Commission Project

Chengdu High-level Key Clinical Specialty Construction Project

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Fig. 1.

Non-heme iron absorption by enterocytes. Duodenal cytochrome B on the apical membrane reduces Fe ${}^{3+}$ to Fe ${}^{2+}$ before divalent metal transporter protein 1 transports Fe ${}^{2+}$ across the apical membrane. Once inside the cell, Fe ${}^{2+}$ can be stored as ferritin, used in various cellular processes, and transported across the basolateral membrane via ferroportin. In the plasma, Fe ${}^{2+}$ is reoxidized by hephaestin and, bound to transferrin, delivered to cells expressing transferrin receptors. Hepcidin, by binding to ferroportin, leads to its internalization and degradation, resulting in decreased iron absorption. Dcytb, duodenal cytochrome B; DMT1, divalent metal transporter protein 1; FPN, ferroportin; Heph, hephaestin; TRF, transferrin.

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Rev. Cardiovasc. Med. Print ISSN 1530-6550 Electronic ISSN 2153-8174