
Atherosclerosis, Год журнала: 2025, Номер 405, С. 119219 - 119219
Опубликована: Май 8, 2025
Patients with cancer treated immune checkpoint inhibitors are at increased risk of myocardial infarction and ischemic stroke. The mechanism is incompletely understood but may involve accelerated atherosclerosis due to enhanced inflammation. Pre-clinical studies provide insight in these mechanisms. To assess the effects modulating co-inhibitory proteins on progression animal models. A systematic review was performed MEDLINE, Embase, Web Science, Scopus up March 2025. Animal were included if effect modulation programmed cell death protein 1 (PD-1), death-ligand (PD-L1), cytotoxic T-lymphocyte associated 4 (CTLA-4), and/or lymphocyte-activation gene 3 (LAG-3) atherosclerotic plaque size evaluated. Secondary outcomes composition systemic ratios means (RoM) across pooled a random meta-analysis. Risk bias assessed using SYRCLE tool, focusing randomization, blinding, completeness outcome reporting. Fourteen eligible included. All used an mouse model (ApoE-/-, Ldlr-/-, ApoE3∗Leiden, or AAV8-PCSK9) either evaluated pharmacological genetic proteins. Upon inhibition, aorta 53 % higher exposed mice compared control (RoM, 1.53; 95 CI, 1.29-1.83; I2 = 89 %). Plaque predominantly characterized by greater abundance CD4+ T cells, CD8+ macrophages. Studies stimulating corroborated findings demonstrated that reduced 28 controls 0.72; 0.65-0.80; 85 This reduction paralleled decrease number macrophages cells plaques. Immune inhibition leads inflammation significant increase murine size. These changes reflect cause stroke patients inhibitors.
Язык: Английский