Related Experiment Video
Updated: Jun 11, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
The Protective Role of Interleukin-37 in Cardiovascular Diseases through Ferroptosis Modulation
Alfredo Cruz-Gregorio1, Luis M Amezcua-Guerra2,3, Brandon Fisher-Bautista2,4
1Departamento de Fisiología, Instituto Nacional de Cardiología Ignacio Chávez, Ciudad de México 14080, Mexico.
Insights
Interleukin-37 protects against cardiovascular diseases by inhibiting ferroptosis, a cell death process linked to iron metabolism. Targeting interleukin-37 offers a potential new therapy for heart conditions.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Death Mechanisms
Background:
- Cardiovascular diseases (CVD) involve complex pathophysiology, with ferroptosis and dysregulated iron metabolism playing significant roles.
- Inflammation is a key driver in CVD, influencing ferroptosis and disease progression.
- Interleukin-37 (IL-37) emerges as a protective cytokine with anti-inflammatory and anti-ferroptotic properties.
Purpose of the Study:
- To review the current understanding of interleukin-37's role in modulating ferroptosis within cardiovascular disease contexts.
- To explore IL-37's mechanisms, including its impact on macrophage ferroptosis and atherosclerosis.
- To highlight the therapeutic potential of targeting IL-37 for CVD prevention and treatment.
Main Methods:
- Literature review of existing studies on IL-37, ferroptosis, and cardiovascular diseases.
- Analysis of IL-37's immunoregulatory functions and its effects on ferroptosis pathways.
- Examination of preclinical data, particularly murine models of atherosclerosis.
Main Results:
- IL-37 activates the nuclear factor erythroid 2-related factor 2 (NRF2) pathway.
- IL-37 inhibits ferroptosis in macrophages.
- IL-37 demonstrates a protective effect against atherosclerosis progression in animal models.
Conclusions:
- Interleukin-37 exhibits significant protective effects against ferroptosis-associated cardiovascular pathology.
- Modulating IL-37 presents a promising therapeutic strategy for cardiovascular diseases.
- Further research into IL-37-targeted therapies could lead to novel treatments for conditions like atherosclerosis and myocardial infarction.
Abstract:
The role of ferroptosis and iron metabolism dysregulation in the pathophysiology of cardiovascular diseases is increasingly recognized. Conditions such as hypertension, cardiomyopathy, atherosclerosis, myocardial ischemia/reperfusion injury, heart failure, and cardiovascular complications associated with COVID-19 have been linked to these processes. Inflammation is central to these conditions, prompting exploration into the inflammatory and immunoregulatory molecular pathways that mediate ferroptosis and its contribution to cardiovascular disease progression. Notably, emerging evidence highlights interleukin-37 as a protective cytokine with the ability to activate the nuclear factor erythroid 2-related factor 2 pathway, inhibit macrophage ferroptosis, and attenuate atherosclerosis progression in murine models. However, a comprehensive review focusing on interleukin-37 and its protective role against ferroptosis in CVD is currently lacking. This review aims to fill this gap by summarizing existing knowledge on interleukin-37, including its regulatory functions and impact on ferroptosis in conditions such as atherosclerosis and myocardial infarction. We also explore experimental strategies and propose that targeting interleukin-37 to modulate ferroptosis presents a promising therapeutic approach for the prevention and treatment of cardiovascular diseases.
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Necrosis
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Myocarditis I: Introduction

