Lysyl oxidase-like 2 inhibition ameliorated podocyte fibrosis by inhibiting transforming growth factor-beta signaling under high-glucose conditions

LOXL2 is upregulated in diabetic podocytes and contributes to hyperglycemia-induced fibrosis by activating the TGF-β/Smad signaling pathway. These findings suggest that LOXL2 may serve as a potential therapeutic target for preventing or attenuating podocyte injury in patients with diabetic nephropathy.