Related Experiment Video
Updated: Jan 16, 2026
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Interleukin-36: a novel therapeutic target for atherosclerosis
Shuting Tan1, Yongheng Li2, Zhenshuai Yao3
1Aging Health Research Center, School of Nursing, Health Science Center, Hunan Normal University, Changsha, 410013, China; The Fourth Hospital of Changsha (Integrated Traditional Chinese and Western Medicine Hospital of Changsha), Changsha, 410006, China.
Insights
Interleukin-36 (IL-36) drives atherosclerosis by promoting vascular inflammation and disrupting cholesterol metabolism. Targeting IL-36 offers a promising strategy to reduce residual cardiovascular disease risk beyond statin therapy.
Area of Science:
- Cardiovascular Science
- Immunology
- Molecular Biology
Background:
- Cardiovascular diseases are a leading cause of death globally, with atherosclerosis as the primary pathology.
- Statin therapy reduces cardiovascular risk but leaves a significant residual risk, necessitating new therapeutic targets.
- Interleukin-36 (IL-36) is an inflammatory cytokine increasingly linked to cardiovascular pathologies.
Purpose of the Study:
- To review the regulatory roles and signaling mechanisms of IL-36 in cardiovascular disease.
- To emphasize IL-36's contribution to atherogenesis and its potential as a therapeutic target.
Main Methods:
- Literature review of recent studies on IL-36.
- Analysis of IL-36's involvement in inflammatory responses within the cardiovascular system.
- Examination of IL-36's impact on key atherogenic processes.
Main Results:
- IL-36 promotes atherosclerosis through sustained vascular inflammation.
- IL-36 contributes to abnormal angiogenesis, impaired cholesterol metabolism, and disrupted autophagy.
- IL-36 signaling exacerbates neutrophil extracellular trap formation.
Conclusions:
- IL-36 plays a significant pro-atherogenic role, contributing to disease initiation and progression.
- IL-36 represents a potential novel therapeutic target for cardiovascular diseases.
- Further research into IL-36 pathways may yield new treatment strategies for atherosclerosis.
Abstract:
Cardiovascular diseases remain the foremost cause of global morbidity and mortality, with atherosclerosis serving as the pathological basis for most related disorders. Despite the clinical benefits of statin therapy, a substantial residual risk persists, underscoring the need to explore novel therapeutic targets. Interleukin-36 (IL-36), a member of the interleukin-1 family, has emerged as a key regulator of immune and inflammatory responses. Beyond its established roles in tissue repair, host defense, and inflammatory signaling, IL-36 has been increasingly implicated in cardiovascular pathology, including myocardial infarction, ischemic injury, and myocarditis. Recent evidence highlights its pro-atherogenic functions mediated through sustained vascular inflammation, abnormal angiogenesis, impaired cholesterol metabolism, excessive neutrophil extracellular trap formation, and disrupted autophagy. These findings collectively suggest that IL-36 not only contributes to the initiation and progression of atherosclerosis but also holds promise as a potential therapeutic target. This review summarizes recent progress on the regulatory roles and signaling mechanisms of IL-36, emphasizing its contribution to atherogenesis.
Related Concept Videos
01:26Atherosclerosis III: Management
01:24T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...