Atherosclerotic Cardiovascular Disease and Cancer
Rattachement africain : us. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Atherosclerotic cardiovascular disease (ASCVD) and cancer are increasingly recognized as interconnected diseases linked by shared immune mechanisms rather than merely overlapping risk factors. Common exposures such as smoking, obesity, diabetes, and dyslipidemia, together with aging and clonal hematopoiesis of indeterminate potential (CHIP), establish a chronic inflammatory milieu that drives both pathologies through coordinated reprogramming of myeloid and lymphoid compartments. Within this framework, a forward cardio-oncology axis is increasingly recognized, in which cancer therapies including chemotherapies, radiation, and immune checkpoint inhibitors induce cardiovascular injury, manifesting as cardiomyopathy, accelerated atherosclerosis, and immune-mediated myocarditis. Complementing this, a reverse axis has emerged in which cardiovascular injury states such as myocardial infarction, ischemia, and heart failure actively promote cancer initiation and progression through hematopoietic remodeling, extracellular vesicle-mediated communication, cardiac-derived factors, and immunosuppressive myeloid bias. At the tissue level, immune checkpoint pathways including PD-1, PD-L1, CTLA-4, LAG-3, and TIM-3 form spatially organized regulatory networks within atherosclerotic plaques. Their therapeutic perturbation restores T cell activity but may disrupt local immune homeostasis and promote plaque instability. In parallel, inflammatory cytokines such as IL-1β, IL-6, and TNF-α, often amplified by CHIP-associated clones, provide a mechanistic bridge linking atherogenesis with tumor immune evasion. Together, these observations support a unified view of ASCVD and cancer as immune-driven diseases connected by bidirectional axes of interaction. This review integrates emerging mechanistic and clinical evidence and outlines how immune-based stratification and targeted modulation of inflammation may enable more precise management of patients at the intersection of cardiovascular disease and cancer.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Atherosclerotic Cardiovascular Disease and Cancer
- Date Crossref
- 01/07/2026
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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NYU Langone Health pays non établi dans la noticeÉtablissement de santé
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New York University pays non établi dans la noticeUniversité ou école supérieure
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Washington University in St. Louis pays non établi dans la noticeUniversité ou école supérieure
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Department of Medicine NYU Grossman School of Medicine New York New York USA Leon H. Charney Division of Cardiology pays non établi dans la noticeUniversité ou école supérieure
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Department of Pathology and Immunology Washington University School of Medicine Saint Louis Missouri USA pays non établi dans la noticeUniversité ou école supérieure
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Department of Medicine Washington University School of Medicine Saint Louis Missouri USA Center for Cardiovascular Research pays non établi dans la noticeUniversité ou école supérieure
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Department of Pathology NYU Grossman School of Medicine New York New York USA pays non établi dans la noticeUniversité ou école supérieure
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Department of Cell Biology NYU Grossman School of Medicine New York New York USA pays non établi dans la noticeUniversité ou école supérieure
NYU Langone Health, New York University et Washington University in St. Louis, avec 5 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.