Authors
Shanshan Liang, Xinyu Wang, Jianxue Zhang, Chuanmin Tao, Wei Gan
Published in
Vascular pharmacology. Pages 107719. Nov 02, 2026. Epub Nov 02, 2026.
Abstract
Immune checkpoint inhibitors(ICIs) improve cancer outcomes but may also perturb vascular immune homeostasis and increase atherosclerotic cardiovascular risk. Clinical cohorts and imaging studies associate ICI exposure with atherosclerotic events, plaque progression, and arterial inflammatory changes, although causality and the relevant vascular phenotype remain incompletely defined. This Review examines a lipoprotein-immune checkpoint interface linking plaque inflammation with antitumor immunity. We focus on low-density lipoprotein(LDL) and oxidized LDL(oxLDL), lipoprotein(a)[Lp(a)] and oxidized phospholipids (OxPLs), statin-related regulation of ubiquitin-like 3(UBL3)-dependent programmed death-ligand 1(PD-L1) sorting into small extracellular vesicles(sEVs), and proprotein convertase subtilisin/kexin type 9(PCSK9). Lp(a) and OxPLs are established atherosclerotic cardiovascular disease(ASCVD) mediators but unvalidated ICI-specific biomarkers. Statins have proven cardiovascular benefit and emerging mechanistic links to PD-L1 trafficking, whereas oncologic associations remain observational. PCSK9 inhibition combines established lipid lowering with preclinical enhancement of antigen presentation and checkpoint response, but randomized ICI-specific evidence is lacking. Current evidence therefore supports a testable translational framework rather than a validated causal axis. Guideline-directed cardiovascular prevention remains the clinical standard while biomarker and therapeutic hypotheses require prospective validation.
PMID:
42971517
Bibliographic data and abstract were imported from PubMed on 03 Nov 2026.
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