Table 1.

Key molecules associated with high glucose in podocytes.

Key Molecules	Effect on Podocytes	Mechanism	Experimental Model	Expression	Ref.
mTORC1	Hypertyophy Foot process effacement GBM thickening podocyte loss	Mislocalization of nephrin, ER stress	db/db mice	increase	[21,22]
PKCα	Foot process effacement	Endocytosis of nephrin	STZ mice DN, human	increase	[30,31]
Integrinα3β	Podocyte detachment	connecting podocytes with the 7GBM	STZ rats DN, human	decrease	[32,33]
NOX4	Foot process effacement	ROS production	ApoE(−/−) mice	increase	[34]
NOX5	Foot process effacement GBM thickening	ROS production	DN, human	increase	[35]
TRPC5	Foot process effacement Podocyte loss	cytoskeletal rearrangement	Dhal SS rats	increase	[36,37]
TRPC6	Podocyte apoptosis	intracellular Ca(2+) overload, NOX4-derived ROS production	Dhal SS rats	increase	[38]
Dnmt1	Foot process effacement	DNA methylation in the nephrin promoter region	db/db mice	increase	[39]
KLF4	Foot process effacement	DNA methylation in the nephrin promoter region	db/db mice DN, human	decrease	[40,41]
KAT5	Foot process effacement	Impaired DNA repair	db/db mice	decrease	[42]

mTORC1: mechanistic target of rapamycin complex1, PKCα: Protein kinase Cα, NOX4: nicotinamide adenine dinucleotide phosphate oxdase4,NOX5: nicotinamide adenine dinucleotide phosphate oxdase5, TRPC5: Transient receptor potential cation channel, subfamily C, member 5, TRPC6: Transient receptor potential cation channel, subfamily C, member 6, Dnmt1: DNA (cytosine-5)-methyltransferase 1, KLF4: Krüppel-like transcription factor 4, GBM: glomerular basement membrane, ER: endoplasmic reticulum, ROS: Reactive Oxygen Species, STZ: Streptozocin, DN: diabetic nephropathy, ApoE(−/−): apo E deficiency, Dhal SS: Dhal salt sensitive.