22 August 2022 : Review article
Programmed Cell Death in Diabetic Nephropathy: A Review of Apoptosis, Autophagy, and Necroptosis
Nour S. Erekat1EF*DOI: 10.12659/MSM.937766
Med Sci Monit 2022; 28:e937766
Table 1 Potential therapeutic implications of apoptosis, autophagy, and necroptosis in diabetic nephropathy.
| Type of programmed cell death | Therapeutic implications | Reference (s) |
|---|---|---|
| Apoptosis | Paricalcitol and/or enalapril attenuated the oxidative stress, and subsequently suppressed apoptosis via reducing the renal expression of pro-apoptotic p53 and caspase-3 and augmenting the expression of the anti-apoptotic Bcl-2 | []140 |
| Catalase overexpression decreased the upregulated p53 gene | [–]141 | |
| Taurine acted as an endogenous antioxidant and attenuated hyperglycemia-induced apoptosis by inhibiting oxidative stress | []144 | |
| miR-27a-3p inhibition slowed the progression of diabetic nephropathy by suppressing podocyte apoptosis via upregulating TIMP3 | []145 | |
| Autophagy | Calorie restriction enhanced renal impairment by repairing autophagy activity | []147 |
| Rapamycin induced autophagy by inhibiting mTORC1 | [,]124 | |
| Metformin and resveratrol induced autophagy by activating AMPK | [–]150 | |
| Necroptosis | Adiponectin decreased the expression levels of RIPK1 and RIPK3 | []156 |
| Nec-1 inhibited the expression of RIPK1 and RIPK3 following the inhibition of apoptosis | []31 | |
| Genetic deletion of UCHL1 decreased the half-life of RIPK1 and RIPK3 proteins and underexpressed RIPK1 and RIPK3 | []31 | |
| Bcl-2 – B-cell lymphoma 2; TIMP3 – tissue inhibitor of matrix metalloproteinases-3; mTORC1 – Mammalian target of rapamycin complex 1; AMPK – adenosine monophosphate-activated protein kinase; Nec-1 – necrostatin-1; RIPK – receptor-interacting serine/threonine kinase; UCHL1 – ubiquitin C-terminal hydrolase L1. | ||