Clinical application of RUBCN/SESN2 mediated inhibition of autophagy as biomarkers of diabetic kidney disease

• Published in: Molecular medicine (Cambridge, Mass.) Mass.), 2022-12, Vol.28 (1), p.147-147, Article 147
• Main Authors: Watany, Mona M, El-Horany, Hemat E, Elhosary, Marwa M, Elhadidy, Ahmed A
• Format: Article
• Language: English
• Subjects: Autophagy; Biomarkers; Cell cycle; Cholesterol; Creatinine; Diabetes; Diabetes Mellitus; Diabetic Nephropathies - diagnosis; Diabetic nephropathy; Endoplasmic reticulum; Glucose; High density lipoprotein; Homeostasis; Humans; Hyperglycemia; Hypoxia; Insulin resistance; Insulin resistance, glycemic control; Kidney diseases; Kinases; Mammalian/mechanistic target of rapamycin (mTOR); Pathogenesis; Phosphorylation; Proteins; Retrospective Studies; RNA, Messenger - genetics; Rubicon (RUBCN); Sestrin-2 (SESN2); Sestrins; Triglycerides
• ISSN: 1076-1551; 1528-3658
• DOI: 10.1186/s10020-022-00580-8

Deregulated autophagy in diabetes has been a field of many experimental studies recently. Impaired autophagy in diabetic kidneys orchestrates every step of diabetic nephropathy (DN) pathogenesis. This study aimed to evaluate three autophagy regulators; RUBCN, mTOR, and SESN2 as clinically applicable indicators of DN progression and as early predictors of DN. This retrospective study included 120 participants in 4 groups; G1: diabetic patients without albuminuria, G2: diabetic patients with microalbuminuria, G3: diabetic patients with macroalbuminuria and G4: healthy controls. RUBCN and SESN2 genes expression were tested by RT-qPCR. RUBCN, mTOR, and SESN2 serum proteins were quantitated by ELISA. RUBCN mRNA was over-expressed in diabetic patients relative to controls with the highest level found in G3 followed by G2 then G1; (9.04 ± 0.64, 5.18 ± 0.73, 1.94 ± 0.41 respectively. P