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Updated: Jun 10, 2026
Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
Published on: May 17, 2015
Cardiac allograft vasculopathy: do adipocytes bridge alloimmune and metabolic risk factors?
Jennifer R Wehner1, William M Baldwin
1Department of Immunology NB30, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Ave, Cleveland, Ohio, USA.
Insights
Cardiac allograft vasculopathy (CAV) is linked to inflammation. Perivascular fat imbalances in cytokines may worsen immune injury in transplanted heart arteries, contributing to graft failure.
Area of Science:
- Immunology
- Cardiology
- Metabolic Science
Background:
- Cardiac allograft vasculopathy (CAV) is a primary cause of chronic graft failure after heart transplantation.
- CAV is characterized by intimal expansion, inflammation, and fibrosis in coronary arteries.
Purpose of the Study:
- To review recent publications linking metabolic and immunologic risk factors for CAV.
- To propose that periarterial adipocytes contribute to immune injury in coronary arteries.
Main Methods:
- Review of clinical and experimental evidence.
- Analysis of cytokine secretion by perivascular adipose tissue.
- Examination of antibody associations with CAV.
Main Results:
- Alloantibodies and autoantibodies are associated with CAV.
- Perivascular adipose tissue releases proinflammatory cytokines (IL-6, IL-8, MCP-1) and less anti-inflammatory adiponectin.
- Adiponectin influences vascular endothelium and reduces neointimal formation.
Conclusions:
- Imbalances in perivascular fat cytokines are implicated in atherosclerosis and restenosis.
- This cytokine imbalance may exacerbate immune responses in transplanted heart coronary arteries.
Purpose Of Review:
Cardiac allograft vasculopathy (CAV) is still a major cause of chronic graft failure. CAV develops in the coronary arteries as a diffuse, concentric expansion of the intima in conjunction with inflammation and fibrosis of the adventitia. We review recent publications that could link metabolic and immunologic risk factors for CAV.A concept is offered that periarterial adipocytes may provide proinflammatory cytokines that augment immune injury of the coronary arteries.
Recent Findings:
Clinical and experimental evidence indicate that some alloantibodies and autoantibodies are associated with CAV. Limited data are available on the expression of target antigens on coronary arteries at different times after transplantation. Perivascular adipose tissue is an abundant source of IL-6, IL-8 and MCP-1. Adding to the inflammatory bias, perivascular adipocytes secrete less of the anti-inflammatory adiponectin in comparison to other types of fat. Adiponectin modulates expression of adhesion molecules on the vascular endothelium. It also decreases neointimal formation in arteries following mechanical endovascular injury.
Summary:
Alterations in the balance between proinflammatory and anti-inflammatory cytokines secreted by perivascular fat have been implicated in atherosclerosis and restenosis. This imbalance may also augment the immune responses in the coronary arteries of transplanted hearts.
