.png){kind=icon}
.png){kind=icon}
Return
Molecular basis of coronary artery disease–malignancy comorbidity: inflammation; immunometabolism; thrombosis; and cardio-oncology translation
.png){kind=icon}
OA
AI
J
Y
M
DOI：10.3389/fimmu.2026.1903190.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Coronary artery disease (CAD) and malignancy frequently coexist in aging populations and share multiple risk factors; including smoking; obesity; diabetes; dyslipidemia; chronic inflammation; and metabolic dysfunction. However; increasing evidence suggests that CAD–malignancy comorbidity cannot be fully explained by epidemiological coincidence alone; although its causal direction remains difficult to establish because of shared risk factors; surveillance bias; reverse causality; cancer stage; and treatment exposure. Instead; convergent inflammatory; metabolic; thrombotic; and immune mechanisms may contribute to the observed clinical overlap. This review summarizes recent evidence linking CAD and cancer through chronic systemic inflammation; clonal hematopoiesis; inflammasome activation; immunometabolic remodeling; endothelial dysfunction; platelet activation; neutrophil extracellular trap formation; coagulation; and immune checkpoint disruption. Particular attention is given to clonal hematopoiesis as a molecular bridge between malignant predisposition and atherosclerosis; macrophage and T-cell immunometabolism as shared immune programs; and thromboinflammation as a mechanism connecting cancer-associated thrombosis with coronary vascular events. We further discuss cardio-oncology translation; including immune checkpoint inhibitor-related cardiovascular toxicity; CHIP-guided anti-inflammatory prevention; antiplatelet and antithrombotic strategies; endothelial-targeted interventions; and immune checkpoint-aware cardiovascular monitoring. Understanding these shared pathways may help move cardio-oncology beyond the management of therapy-induced cardiotoxicity toward mechanism-guided prevention and treatment of inflammatory; thrombotic; and immune mechanisms that jointly promote CAD progression and cancer development.
Keywords:
clonal hematopoiesis
immunometabolism
malignancy
coronary artery disease
cardio-oncology
Journal
IF:
5.9
Papers:
4.9W
Citations:
22.7W
Organization
No organization information available
Cited Papers