Abstract
Glomerular podocytes are highly differentiated cells that cover glomerular capillaries from the outside and have a characteristic morphology with numerous foot processes. The formation of slit membranes between the foot processes serves as a final filtration barrier for urine filtration from the blood. Podocyte damage causes disruption of the slit membrane, subsequent proteinuria and finally glomerulosclerosis, which is a common pathway in various types of chronic kidney disease (CKD). In recent years, there has been an increase in diabetes, due to rapid lifestyle changes, which is the main cause of CKD. Therefore, understanding the effect of diabetic status on podocytes is of great importance to establish a strategy for preventing CKD progression. In this review, we summarize altered glucose and lipid metabolism in diabetic podocytes and also discuss the reversibility of the changes in podocyte phenotype.
Highlights
This review summarizes podocyte injury in diabetes, focusing on the effect of high glucose itself, and lipotoxicity that is frequently associated with diabetes
Several studies have suggested that Mechanistic Target of Rapamycin Signaling Complex 1 (mTORC1), a kinase that senses nutrient availability, was upregulated in podocyte of diabetic mice, and closely associated with the activation of podocyte hypertrophy induced by high glucose [21]
Podocyte apoptosis under high-glucose conditions is associated with the release of mitochondrial and plasma membrane reactive oxygen species (ROS) that trigger the p38MAPK and nicotinamide adenine dinucleotide phosphate oxidases (NOX) signaling pathways [46,47]
Summary
It has recently become clear that the initial glomerular injury affects the podocytes as important target cells for the progression of CKD and end-stage kidney disease [5]. As podocytes are terminally differentiated cells without a capacity for proliferation or replenishment, chronic injury causes phenotypical changes, detachment and apoptosis in podocytes, leading to disruption of the slit membrane and glomerulosclerosis [6,7]. Understanding podocyte phenotype and function in diabetes is necessary for CKD management and for considering future therapeutic targets. Improvement in HbA1c decelerates glomerular filtration rate (GFR) loss and delays the onset of End stage renal diseases (ESRD) in patients with type 1 diabetes mellitis (T1DM).
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