Protective Effect of Aldo–keto Reductase 1B1 Against Neuronal Cell Damage Elicited by 4′-Fluoro-α-pyrrolidinononanophenone

JOURNAL/nrgr/04.03/01300535-202403000-00034/inline-graphic1/v/2023-08-11T153926Z/r/image-tiff Diabetic peripheral neuropathy is a common complication of diabetes mellitus. Elucidating the pathophysiological metabolic mechanism impels the generation of ideal therapies. However, existing limited treatments for diabetic peripheral neuropathy expose the urgent need for cell metabolism research. Given the lack of comprehensive understanding of energy metabolism changes and related signaling pathways in diabetic peripheral neuropathy, it is essential to explore energy changes and metabolic changes in diabetic peripheral neuropathy to develop suitable treatment methods. This review summarizes the pathophysiological mechanism of diabetic peripheral neuropathy from the perspective of cellular metabolism and the specific interventions for different metabolic pathways to develop effective treatment methods. Various metabolic mechanisms (e.g., polyol, hexosamine, protein kinase C pathway) are associated with diabetic peripheral neuropathy, and researchers are looking for more effective treatments through these pathways.

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Protective Effect of Aldo–keto Reductase 1B1 Against Neuronal Cell Damage Elicited by 4′-Fluoro-α-pyrrolidinononanophenone

Cited by 3 publications

References 45 publications

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Linarin ameliorates ischemia-reperfusion injury by the inhibition of endoplasmic reticulum stress targeting AKR1B1

Liraglutide alleviated alpha-pyrrolidinovalerophenone (α-PVP) induced cognitive deficits in rats by modifying brain mitochondrial impairment

Cell metabolism pathways involved in the pathophysiological changes of diabetic peripheral neuropathy

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