Table 4.

Regulatory Mechanism of Nox4 in Diabetic neuropathy.

Models	Intervention	Regulating factors/Signal pathways	Main results	Conclusion	Reference
The schwann cells of newborn Wistar rats were cultured in vitro	siRNA-Nox4 treatment	Nox4/ROS	ROS↓, Caspase-3↓, Oxidative stress↓, Apoptosis↓	Effective inhibition of Nox4 can be a protective strategy for developing drugs for diabetic peripheral neuropathy.	[123]
T1DM mice, high glucose-stimulated Schwann cells, and T2DM patient skin biopsies	Targeted activation of LXR or specific inhibition of Nox4	LXR/Nox4	LXR↑, Nox4↓, ROS↓, neurophysiological defects↓, sensorimotor abnormalities↓, and defective peripheral myelin gene expression↓	Targeting the LXR/Nox4 axis is a promising therapeutic approach for diabetic peripheral neuropathy.	[127]
Human skin microvascular endothelial cells	DA-9801 treatment	Nox4/p22/Ang II	Nox4↓, p22↓, Ang II↓, Oxidative stress↓	To explore the pathogenesis of Nox4 in diabetic or hyperglycemic peripheral microangiopathy and to provide a theoretical basis for finding key targets.	[128]