Interleukin-10 as a central immunoregulatory mediator in cardiovascular diseases: A systematic review of mechanistic insights, clinical significance and therapeutic potential

Cardiovascular (CV) diseases (CVDs) have shifted from being hypothesized as lipid-driven disorders, to now chronic immune-mediated inflammatory disorders. Vascular inflammation has been shown to be a key mediator of endothelial dysfunction, subsequent atheroma development and progression (including plaque destabilization) and subsequent vascular events in the pathophysiology of cardiovascular disease (CVD).
Because of its potent immunoregulatory qualities, interleukin-10 (IL-10) is one of the most universal anti-inflammatories, multifunctional cytokines that promotes vascular immune system homeostasis. The current comprehensive review aims to critically evaluate the molecular underpinnings, clinical correlations, and possible therapeutic implications of IL-10 in cardiovascular disorders.
Methods: A systematic review that searched PubMed, Scopus, and Web of Science between 2020 and 2025 found 1247 papers, 42 of which satisfied the inclusion criteria. Strong evidence supports the cardioprotective effects of IL-10 by inhibiting pro-inflammatory cytokines (TNF-α, IL-6, and IL1β) and the NF-κB signaling pathway. This improves endothelial function and may modulate macrophage polarization toward M2 phenotype, which affects the stabilization of atherosclerotic plaque.
Low IL-10 has been clinically linked to higher cardiovascular risk and a worse prognosis in patients with heart failure and myocardial infarction, as evidenced by elevated systemic inflammation. However, problems with systemic immunosuppression and pharmacokinetics are the principal obstacles to therapeutic translation.
IL-10 could serve as a novel biomarker and therapeutic target in personalized cardiovascular medicine, although the clinical evidence needs to be confirmed by large-scale randomized trials.