Overview of key molecular processes behind diabetic nephropathy

Selim, Salma Mohamed; Hazem, Reem; Elfayoumi, Hassan Mahmoud Mohamed; El-Sayed, Norhan Mohamed

doi:10.21608/rpbs.2025.366022.1363

	Overview of key molecular processes behind diabetic nephropathy
Records of Pharmaceutical and Biomedical Sciences
Volume 9, Issue 3, March 2025, Page 32-39 PDF (543.11 K)
Document Type: Mini-reviews
DOI: 10.21608/rpbs.2025.366022.1363
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Authors
Salma Mohamed Selim ¹; Reem Hazem ²; Hassan Mahmoud Mohamed Elfayoumi³; Norhan Mohamed El-Sayed ²
¹Pharmacology and toxicology, Faculty of Dentistry, Sinai University
²Department of Pharmacology & Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt.
³Department of Pharmacology & Toxicology, Faculty of Dentistry, Sinai University, Kantara, Ismailia 41635, Egypt.
Abstract
Diabetic nephropathy (DN) is one of the diabetic chronic microvascular consequences and a leading cause of end-stage renal disease (ESRD). DN is defined by hyperfiltration and albuminuria in the early stages, followed by gradual renal function deterioration. The appearance of diabetic kidney disease (DKD) might vary, especially in individuals with type 2 diabetes mellitus, where the concurrent presence of various glomerular/tubular pathologies and severe peripheral vascular disease can become key confounding factors. The fundamental question in the current review is "What is the primary mechanism leading to the pathology of DN?" This review discusses the molecular processes that cause oxidative stress (OS), hypoxia, dysregulated autophagy and apoptosis, and epigenetic alterations causing kidney inflammation and fibrosis, ultimately leading to progressive renal scarring and dysfunction. Additionally, it examines the interplay between metabolic abnormalities, mitochondrial dysfunction, endothelial damage, and pro-inflammatory cytokines, which contribute to the complex pathophysiology of DN and further accelerate renal deterioration.
Keywords
Diabetic kidney disease; oxidative stress; inflammation; apoptosis; and autophagy


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