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Life sciences · Journal article
Respiratory Research · November 3, 2026
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Respiratory diseases and atherosclerotic cardiovascular disease (ASCVD) frequently coexist in aging populations, yet the field is still dominated by parallel descriptions of pulmonary and vascular mechanisms rather than an integrated explanation of how lung pathology is translated into arterial injury. In this review, we propose a lung–blood–artery axis as the central conceptual framework linking respiratory disease to atherosclerosis. In this model, a shared susceptibility terrain—comprising aging, cellular senescence, smoking-related injury, oxidative stress, and metabolic dysfunction—primes both the respiratory system and the vasculature. Disease-specific respiratory triggers, including chronic airway or alveolar inflammation, intermittent hypoxia, fibrotic remodelling, type 2/allergic inflammation, chronic infection, and tumour- or therapy-related immune activation, then generate systemic signals that extend beyond the lung. These signals are transmitted through circulating cytokines and acute-phase reactants, extracellular vesicles, oxidized lipids, activated leukocytes and platelets, and neurohumoral pathways, and converge on endothelial dysfunction, innate immune amplification, disturbed lipid handling, oxidative stress, and cellular senescence within the arterial wall. This framework clarifies why different respiratory phenotypes can converge on common vascular outcomes while still differing in evidentiary strength. Current evidence is strongest for chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea, in which systemic inflammation, hypoxia-related vascular stress, and endothelial injury have substantial epidemiological, functional, and mechanistic support. In interstitial lung disease, asthma, bronchiectasis, and lung cancer, the association is increasingly supported, but the degree of cross-organ causal validation varies and, in some contexts, remains inferential. Framing respiratory–atherosclerotic multimorbidity in this way shifts the emphasis from organ-specific pathway cataloguing to translatable disease modules and therapeutic nodes. It also helps distinguish upstream respiratory triggers from downstream vascular effectors, thereby providing a more precise rationale for multimorbidity-oriented prevention and treatment strategies.