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Life sciences · Journal article
Biomedicines · October 22, 2026
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Cardiometabolic disease, encompassing hypertension, type 2 diabetes, obesity, and dyslipidemia, is the predominant driver of cardiovascular disease (CVD) morbidity and mortality worldwide, and the vascular endothelium sits at the transition from metabolic derangement to overt cardiovascular events, serving as both sensor and transducer of metabolic injury. This review synthesizes evidence that aberrant immune responses act as contributory drivers of endothelial injury in cardiometabolic disease. These responses span innate pattern-recognition receptor activation, neutrophil-mediated cytotoxicity, monocyte/macrophage polarization imbalance, adaptive T- and B-cell dysregulation, and trained immunity. The inflammation they represent is therapeutically actionable at the level of cardiovascular events. Whether endothelial protection mediates that benefit has not been directly tested, and reverse causation and parallel metabolic–inflammatory loops are not excluded. We trace how the canonical innate sensing cascades (Toll-like receptor 4–nuclear factor κB, the NLRP3 inflammasome, and cyclic GMP–AMP synthase–stimulator of interferon genes) converge on endothelial activation. We then examine how oxidative stress at the immune–metabolic interface, including NADPH oxidase-derived reactive oxygen species, endothelial nitric oxide synthase uncoupling, mitochondrial damage-associated molecular pattern release, and oxidized phospholipid accumulation, amplifies this convergence. Finally, we describe how junctional disassembly, glycocalyx degradation, and endothelial-to-mesenchymal transition execute barrier disruption. We then assess mechanism-linked circulating biomarkers and multi-marker integration strategies, anchoring the framework in clinical trials that have established anti-inflammatory therapy in selected patient populations while the mechanistic steps linking these interventions to endothelial protection remain incompletely tested. We close by consolidating this evidence into a graded inventory that separates candidate circulating readouts from intervention and real-world evidence, and by marking where the mechanistic chain from pathway to readout to therapy remains unclosed. Whether these pathways can be translated into mechanism-informed risk stratification awaits prospective evidence and standardized measurement.