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	[141–143]
	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	[124,148]
	Metformin and resveratrol induced autophagy by activating AMPK	[150–153]
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.