Preprint Review Version 1 This version is not peer-reviewed

Protective Role of Interleukin-37 via Ferroptosis in Cardiovascular Diseases

Version 1 : Received: 30 July 2024 / Approved: 31 July 2024 / Online: 31 July 2024 (10:24:23 CEST)

How to cite: Cruz-Gregorio, A.; Amezcua-Guerra, L. M.; Fisher-Bautista, B. U.; Romero-Beltrán, A.; Fonseca-Camarillo., G. Protective Role of Interleukin-37 via Ferroptosis in Cardiovascular Diseases. Preprints 2024, 2024072521. https://doi.org/10.20944/preprints202407.2521.v1 Cruz-Gregorio, A.; Amezcua-Guerra, L. M.; Fisher-Bautista, B. U.; Romero-Beltrán, A.; Fonseca-Camarillo., G. Protective Role of Interleukin-37 via Ferroptosis in Cardiovascular Diseases. Preprints 2024, 2024072521. https://doi.org/10.20944/preprints202407.2521.v1

Abstract

Ferroptosis and dysregulation of iron metabolism are increasingly recognized as contributors to the onset and development of cardiovascular diseases (CVD), including hypertension, cardiomyopathy, atherosclerosis, pulmonary hypertension, myocardial ischemia/reperfusion injury, heart failure, and cardiovascular manifestations of Coronavirus disease 19 (COVID-19). In-flammation plays a central role in these conditions, prompting exploration into the inflammatory and immunoregulatory molecular mechanisms un-derlying ferroptosis and its contribution to CVD progression. In particular, emerging evidence suggests that interleukin (IL)-37 is a protective cytokine capable of activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, suppressing macrophage ferroptosis, and activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway to attenuate atherosclerosis progression in murine models. Despite this, a comprehensive review detailing IL-37 and its protective role against ferroptosis in CVD is absent in the current literature. Thus, this review consolidates the current state of knowledge on IL-37, summarizing its regulatory functions and modulation of ferroptosis in diseases such as atherosclerosis, myocardial infarction, aneurysm, stroke, and other CVD. We also discuss experimental approaches and propose that tar-geting IL-37 to regulate ferroptosis holds promise as a therapeutic strategy in preventing and treating diverse CVD.

Keywords

Interleukin-37; ferroptosis; macrophages; atherosclerosis; cardiovascular diseases; inflammation

Subject

Medicine and Pharmacology, Cardiac and Cardiovascular Systems

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