Diabetes mellitus is one of the biggest public health issues of modern society, with a constant increase in prevalence. It is a complex metabolic disorder characterized by hyperglycemia, dyslipidemia, and impaired insulin signaling, leading to redox imbalance and, consequently, blood vessel dysfunction. One of the key factors in the regulation of vascular tone and contractility is the sodium/potassium adenosine triphosphatase (Na+/K+-ATPase), whose reduced expression and altered activity contribute to the development of vascular dysfunction in type 2 diabetes (T2D). Impaired redox balance and increased production of reactive oxygen species, which directly affect Na+/K+-ATPase activity, also affect the telomere-telomerase system, leading to telomere shortening, DNA damage, and cell apoptosis. Hyperbaric oxygen therapy is used to treat ischemic lesions and vascular complications of diabetes, but the molecular mechanisms underlying its effects on Na+/K+-ATPase and telomere length in T2D patients remain incompletely elucidated.
Zafirović et al. (2026) studied this question.