What cellular mechanisms are involved in the pathophysiology of common chronic diseases such as diabetes and hypertension?

Common chronic diseases such as diabetes mellitus and hypertension share key cellular mechanisms involving endothelial dysfunction, oxidative stress, inflammation, and altered cellular signalling pathways. In hypertension, endothelial dysfunction is central, characterised by impaired nitric oxide bioavailability leading to vasoconstriction and increased vascular resistance ¹. This dysfunction arises from oxidative stress and inflammation within vascular endothelial cells, promoting vascular remodelling and stiffness ¹. Similarly, in diabetes mellitus, particularly type 2, chronic hyperglycaemia induces oxidative stress and inflammatory responses at the cellular level, damaging endothelial cells and pancreatic beta cells, impairing insulin secretion and action (Młynarska et al., 2025). Insulin resistance in peripheral tissues is driven by disrupted intracellular signalling pathways, including impaired insulin receptor substrate activity and downstream effects on glucose transport (Młynarska et al., 2025). Additionally, endothelial dysfunction in diabetes contributes to microvascular complications and is exacerbated by chronic inflammation and oxidative stress (McElwain et al., 2020). Both diseases involve maladaptive cellular responses to metabolic and haemodynamic stressors, resulting in progressive tissue damage and organ dysfunction. Thus, the pathophysiology of diabetes and hypertension converges on cellular mechanisms of endothelial injury, oxidative stress, inflammation, and disrupted signalling pathways that impair vascular and metabolic homeostasis ¹; (McElwain et al., 2020); (Młynarska et al., 2025).