Cannabinoid-1 receptor deletion in podocytes mitigates both glomerular and tubular dysfunction in a mouse model of diabetic nephropathy.

Tony JourdanJoshua K ParkZoltán V VargaJános PálócziNathan J CoffeyAvi Z RosenbergGrzegorz GodlewskiResat CinarKen MackiePal PacherGeorge Kunos

Published in: Diabetes, obesity & metabolism (2017)

Activation of CB1 R in podocytes contributes to both glomerular and tubular dysfunction in type-1 DN, which highlights the therapeutic potential of peripheral CB1 R blockade.

Keyphrases

diabetic nephropathy
high glucose
mouse model
oxidative stress
endothelial cells
radiation therapy
binding protein