Emerging insights into inflammation-driven atherosclerosis: immune cell mechanisms

Area of Science:

• Cardiovascular Science
• Immunology
• Molecular Biology

Background:

• Atherosclerosis is a chronic inflammatory disease characterized by arterial lipid deposition and plaque formation.
• Endothelial activation initiates the process, leading to inflammatory cell infiltration and atheromatous plaque development.
• Existing knowledge lacks a comprehensive integration of immune cell interactions and systemic factors.

Purpose of the Study:

• To review and integrate emerging concepts in the immune cascade of atherosclerosis.
• To detail the interactions of various immune cells within developing plaques using single-cell omics data.
• To explore novel insights like smooth muscle cell plasticity and clonal hematopoiesis, and the impact of systemic factors.

Main Methods:

• Review of current literature on atherosclerosis pathogenesis.
• Integration of findings from single-cell omics studies.
• Analysis of systemic and environmental factors influencing disease progression.

Main Results:

• Immune cells (macrophages, T cells, B cells, DCs, neutrophils) sustain plaque inflammation.
• Vascular smooth muscle cells can adopt macrophage-like phenotypes, contributing to foam cell formation.
• Systemic factors like gut microbiota, epigenetics, hypertension, diabetes, obesity, and smoking exacerbate disease via trained immunity and meta-inflammation.

Conclusions:

• Atherosclerosis is a complex inflammatory disease driven by intricate immune cell crosstalk and systemic influences.
• Novel concepts like smooth muscle cell phenotypic switching and clonal hematopoiesis offer new perspectives.
• Targeting inflammatory axes, considering systemic and environmental factors, is crucial for future therapeutic strategies.