Inflammation as a Unifying Axis: Shared Pathogenic Mechanisms in Coronary Atherosclerosis and Chronic Atrophic Gastritis

Abstract

Abstract Coronary atherosclerosis (AS) and chronic atrophic gastritis (CAG) are clinically distinct diseases but share core features of chronic, non-resolving inflammation. This review evaluates their convergent immunoinflammatory architecture and discusses how shared pathogenic nodes may inform dual-purpose therapeutic strategies. Both conditions involve barrier dysfunction driven by oxidative stress and nitric oxide dysregulation, maladaptive immune responses involving macrophage polarization and T-cell plasticity, and sustained inflammatory signaling through pathways such as TLR/NF-κB, HIF, and PI3K/AKT. Inflammation-driven cellular reprogramming - vascular smooth muscle cell phenotypic switching in AS and gastric glandular atrophy/metaplasia in CAG - links chronic inflammation to clinically important outcomes, including plaque destabilization and gastric carcinogenesis. This mechanistic convergence is clinically relevant when CAD and CAG coexist. Intensive antithrombotic therapy increases gastrointestinal bleeding risk and often requires PPI prophylaxis; however, long-term PPI use may aggravate the progression of atrophic gastritis and gastric precancerous lesions in susceptible patients. We therefore discuss inflammation-targeted strategies as possible candidate approaches to balance cardiovascular protection, gastrointestinal safety, and gastric oncologic risk in this comorbid setting.