Glomerular Autophagy in Diabew: Comparison
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Please note this is a comparison between Version 1 by Anton I. Korbut and Version 4 by Rita Xu.

Glomerular injury is a central feature of diabetic nephropathy. A growing body of evidence indicates a critical role of autophagy in maintaining podocyte integrity and renal function. This process is vital for highly differentiated post-mitotic cells, such as neurons and podocytes. Sodium-glucose cotransporter-2 (SGLT2) inhibitors and dipeptidylpeptidase-4 (DPP4) inhibitors are promising antidiabetic agents introduced into clinical practice in the last decade. The effect of SGLT2 and DPP4 inhibition on glomerular autophagy has not been studied yet. This entry summarizes the study, which have demonstrated, that the SGLT2 inhibitor empagliflozin, the DPP4 inhibitor linagliptin, and a combination of these agents, could reactivate glomerular autophagy in db/db mice, a model of type 2 diabetes. The effect is associated with mitigation of renal hypertrophy, an improvement in glomerular morphology, including a decrease in the severity of podocytopathy, and a slowdown in the growth of albuminuria.

Recent data have indicated the emerging role of glomerular autophagy in diabetic kidney disease. We aimed to assess the effect of the SGLT2 inhibitor empagliflozin, the DPP4 inhibitor linagliptin, and their combination, on glomerular autophagy in a model of type 2 diabetes. Eight-week-old male db/db mice were randomly assigned to treatment with empagliflozin, linagliptin, empagliflozin–linagliptin or vehicle for 8 weeks. Age-matched non-diabetic db/+ mice acted as controls. To estimate glomerular autophagy, immunohistochemistry for beclin-1 and LAMP-1 was performed. Podocyte autophagy was assessed by counting the volume density (VV) of autophagosomes, lysosomes and autolysosomes by transmission electron microscopy. LC3B and LAMP-1, autophagy markers, and caspase-3 and Bcl-2, apoptotic markers, were evaluated in renal cortex by western blot. Vehicle-treated db/db mice had weak glomerular staining for beclin-1 and LAMP-1 and reduced VV of autophagosomes, autolysosomes and lysosomes in podocytes. Empagliflozin and linagliptin, both as monotherapy and in combination, enhanced the areas of glomerular staining for beclin-1 and LAMP-1 and increased VV of autophagosomes and autolysosomes in podocytes. Renal LC3B and Bcl-2 were restored in actively treated animals. LAMP-1 expression was enhanced in the empagliflozin group; caspase-3 expression decreased in the empagliflozin–linagliptin group only. Mesangial expansion, podocyte foot process effacement and urinary albumin excretion were mitigated by both agents. The data provide further explanation for the mechanism of the renoprotective effect of SGLT2 inhibitors and DPP4 inhibitors in diabetes.

  • autophagy
  • podocyte
  • type 2 diabetes
  • diabetic nephropathy
  • empagliflozin
  • linagliptin
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