Markers of cell stress and endothelial dysfunction as components of diagnosis of type 2 diabetes mellitus and obesity
Introduction. This study focuses on the diagnostic role of markers of cellular stress and endothelial dysfunction in patients with type 2 diabetes mellitus and obesity. Cellular stress and endothelial dysfunction are key pathophysiological mechanisms that contribute to the progression of these diseases. We analyzed the general block (gender, age), anthropometric block (height, weight, BMI, waist circumference, fat mass, fat percentage, free fat mass, total, amount of water), anamnestic block (the fact of coronary heart disease onset, the time of coronary heart disease onset, the duration of diabetes mellitus, the fact of smoking), lipid profile data were taken into account (total cholesterol, HDL, LDL, TG), analyzed the level of various biomarkers associated with cellular stress (HSP70, HSP27) and the state of the endothelium (endothelin, stable metabolites of NO, ADMA, hs-CRP) in a group of patients with diabetes and obesity, with diabetes, in the control group. The findings of the study emphasize the importance of assessing markers of cellular stress and endothelial dysfunction as potential diagnostic tools for early diagnosis and monitoring of the condition of patients with type 2 diabetes mellitus and obesity. These findings may facilitate the development of more targeted strategies for the treatment and prevention of cardiovascular disease in this patient group.
Authors
- А. С. Литвинов (ORCID: https://orcid.org/0000-0001-5251-145X)
- D. Yu. Bugrimov (ORCID: https://orcid.org/0000-0002-4763-4153)
- Julia Kotova
- Valeria Dugusheva
- Olga Krasnorutskaya
- Anna Morozova
- Sofia Strelnikova
Publication Details
- Journal
- Medical Scientific Bulletin of Central Chernozemye (Naučno-medicinskij vestnik Centralʹnogo Černozemʹâ)
- Published
- 2025-04-07
- DOI
- https://doi.org/10.18499/1990-472x-2025-26-1-110-114
- Primary Topic
- Adipokines, Inflammation, and Metabolic Diseases
- Type
- article
- Field-Weighted Citation Impact
- 0.00