Ingkar Okhas
Research Subjects
Ingkar Okhas has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Altynay Safiollayeva
City Polyclinic No. 19, Public Health Department of Almaty, Almaty 050054, Kazakhstan
1 shared publication - Arailym Yessenbekova
Department of Biophysics, Biomedicine and Neuroscience, Al-Farabi Kazakh National University, Al-Farabi av. 71, Almaty 050040, Kazakhstan
1 shared publication - Arman Abaildayev
Department of Chemical and Biochemical Engineering, Geology and Oil-Gas Business Institute Named after K. Turyssov, Satbayev University, Almaty 050043, Kazakhstan
1 shared publication - Ayauly Duisenbek
Department of Biophysics, Biomedicine and Neuroscience, Farabi University, Al-Farabi Av. 71, Almaty 050040, Kazakhstan
1 shared publication - Beibarys Mukhitdin
Laboratory of Physiology Lymphatic System, Institute of Genetics and Physiology SC MSHE RK, Almaty 050040, Kazakhstan
1 shared publication - Botagoz Ussipbek
Department of Biophysics, Biomedicine and Neuroscience, Farabi University, Al-Farabi Av. 71, Almaty 050040, Kazakhstan
1 shared publication
Latest Publications
- Open Access
- 18 July 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (14) , 6394
Urinary Extracellular Vesicle-Derived miRNAs as Regulators and Biomarkers in Diabetic Kidney Disease
Diabetic kidney disease (DKD) remains one of the most severe microvascular complications of type 2 diabetes mellitus (T2DM) and a leading cause of chronic kidney disease (CKD) worldwide. Nevertheless, despite considerable progress in elucidating its molecular background, early diagnosis and accurate stratification of disease progression remain challenging when relying on conventional clinical biomarkers such as albuminuria and estimated glomerular filtration rate (eGFR). Growing evidence indicates that DKD is driven by interconnected pathogenic mechanisms, including chronic hyperglycemia, activation of the protein kinase C (PKC) signaling pathway, renin–angiotensin–aldosterone system (RAAS) dysregulation, oxidative stress, inflammatory cascades, and immune system activation involving Toll-like receptors (TLR) and the NLRP3 inflammasome. These processes collectively contribute to endothelial dysfunction, podocyte injury, extracellular matrix accumulation, and progressive renal fibrosis. Exosomes and their molecular cargo, particularly miRNAs, have emerged as promising regulators and non-invasive biomarkers reflecting ongoing renal injury. Urinary exosomal microRNAs (uEV-miRNAs) are of interest due to their stability in biological fluids and their direct origin from nephron segments, enabling real-time reflection of renal pathophysiology. Accumulating studies suggest that differentially expressed microRNAs (miRNAs), including miR-21-5p, miR-30a-5p, miR-192-5p, and miR-142-3p, are closely associated with key pathways in DN. However, their clinical translation remains limited by methodological heterogeneity, the lack of standardized isolation protocols, and insufficient validation in large longitudinal cohorts. This review navigates the current landscape of knowledge on the molecular mechanisms underlying DKD and examines the emerging role of uEV-miRNAs as diagnostic biomarkers. Altogether, uEV-miRNAs offer a promising avenue for improving early detection, risk stratification, and disease monitoring in DKD.
- 18 July 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (14) , 6394
Open AccessUrinary Extracellular Vesicle-Derived miRNAs as Regulators and Biomarkers in Diabetic Kidney Disease
Diabetic kidney disease (DKD) remains one of the most severe microvascular complications of type 2 diabetes mellitus (T2DM) and a leading cause of chronic kidney disease (CKD) worldwide. Nevertheless, despite considerable progress in elucidating its molecular background, early diagnosis and accurate stratification of disease progression remain challenging when relying on conventional clinical biomarkers such as albuminuria and estimated glomerular filtration rate (eGFR). Growing evidence indicates that DKD is driven by interconnected pathogenic mechanisms, including chronic hyperglycemia, activation of the protein kinase C (PKC) signaling pathway, renin–angiotensin–aldosterone system (RAAS) dysregulation, oxidative stress, inflammatory cascades, and immune system activation involving Toll-like receptors (TLR) and the NLRP3 inflammasome. These processes collectively contribute to endothelial dysfunction, podocyte injury, extracellular matrix accumulation, and progressive renal fibrosis. Exosomes and their molecular cargo, particularly miRNAs, have emerged as promising regulators and non-invasive biomarkers reflecting ongoing renal injury. Urinary exosomal microRNAs (uEV-miRNAs) are of interest due to their stability in biological fluids and their direct origin from nephron segments, enabling real-time reflection of renal pathophysiology. Accumulating studies suggest that differentially expressed microRNAs (miRNAs), including miR-21-5p, miR-30a-5p, miR-192-5p, and miR-142-3p, are closely associated with key pathways in DN. However, their clinical translation remains limited by methodological heterogeneity, the lack of standardized isolation protocols, and insufficient validation in large longitudinal cohorts. This review navigates the current landscape of knowledge on the molecular mechanisms underlying DKD and examines the emerging role of uEV-miRNAs as diagnostic biomarkers. Altogether, uEV-miRNAs offer a promising avenue for improving early detection, risk stratification, and disease monitoring in DKD.