Metabolic and Immune Crosstalk in Cardiovascular Disease

Area of Science:

• Cardiovascular biology
• Immunometabolism
• Vascular biology

Background:

• Cardiovascular diseases (CVDs) like atherosclerosis and heart failure result from complex metabolic, immune, and neural dysregulation.
• Endothelial cells in cardiac vessels and lymphatics play crucial roles in regulating cardiac metabolism and tissue homeostasis.
• Dysfunction in these systems, particularly lymphatics and vascular endothelium, exacerbates CVD progression and outcomes.

Purpose of the Study:

• To review recent advances in the metabolic and immune crosstalk within the cardiac vasculature.
• To explore how these interactions influence cardiometabolic health and disease.
• To highlight the role of neuroimmune hubs and T cell plasticity in CVD pathogenesis.

Main Methods:

• Literature review integrating recent findings on endothelial cell metabolism, lymphatic function, and neuroimmune interactions in the heart.
• Analysis of the role of T cells and tertiary lymphoid organs in atherosclerosis.
• Examination of systemic immune activation effects on CVD.

Main Results:

• Coronary and lymphatic endothelial cell dysfunction is a key factor in CVD.
• Lymphatic maladaptation worsens outcomes in metabolic diseases.
• Altered vascular metabolism drives inflammation, fibrosis, and cardiac remodeling in heart failure.
• Artery tertiary lymphoid organs act as neuroimmune hubs promoting atherosclerosis via T cell activation and neurovascular signaling.
• Proinflammatory T cell subsets exacerbate atherosclerosis, influenced by systemic immunity.

Conclusions:

• Integrated therapeutic strategies targeting endothelial metabolism, lymphatic function, neuroimmune crosstalk, and T cell plasticity are promising for managing CVD.
• Understanding the interplay between metabolism, immunity, and neural regulation is critical for novel CVD treatments.