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Selective inhibition of monoamine oxidase B represents a therapeutic strategy for diabetic peripheral neuropathy

Acta Pharmacologica Sinica (2026)Cite this article

Abstract

Diabetic peripheral neuropathy (DPN), a severe complication of diabetes, is a key risk factor for diabetic foot (DF) that contributes highly to amputation and mortality. The pathogenesis of DPN remains unclear and complex, with no effective treatments currently available. Monoamine oxidase (MAO), a flavin adenine dinucleotide (FAD)-dependent enzyme, catalyzes the oxidative deamination of critical biogenic amines. The MAO family comprises two subtypes, MAOA and MAOB, which play distinct roles in pathophysiology. In this study, we identified that MAOB but not MAOA is pathologically upregulated in the sciatic nerve (SN) tissues of DPN patients and in the SN/dorsal root ganglion (DRG) tissues of DPN model mice. Notably, the selective MAOB inhibitor Khellin (Khe) effectively alleviated DPN-like pathology in mice. To explore the mechanistic role of MAOB in DPN, we performed proteomic profiling of DRG tissues from DPN mice and validated the findings using a MAOB-specific knockdown DPN mice model treated with adeno-associated virus (AAV) 8-MAOB-RNAi. Our results demonstrate that Khe targets MAOB to mitigate DPN pathology through HIF-1α/BACE1/Aβ/NLRP3/tau pathway, mediated by Schwann cell/DRG neuron crosstalk. All findings suggest that selective MAOB inhibition represents a promising therapeutic strategy for DPN, with Khe as a potential candidate for clinical translation against this disease.

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Fig. 1: Proteomics analysis revealed the selective and pathological elevation of MAOB expression level in DPN pathology.
Fig. 2: Khe targeted MAOB to ameliorate neurological dysfunctions in DPN mice.
Fig. 3: Khe targeted MAOB to improve the peripheral vascular dysfunction and nerve damage in DPN mice.
Fig. 4: Khe targeted MAOB to protect myelin sheath structure and improve DRG neuronal damage in DPN mice.
Fig. 5: Khe targeted MAOB to inhibit DRG neuronal tau hyperphosphorylation in DPN mice.
Fig. 6: Khe targeted MAOB to suppress tau hyperphosphorylation through Aβ/NLRP3 axis by Schwann cell/DRG neuron crosstalk.
Fig. 7: Khe targeted MAOB to alleviate Aβ/NLRP3 axis in SN tissues of DPN mice and to suppress Aβ level through HIF-1α/BACE1 axis in DPN mice.
Fig. 8: HIF-1α/BACE1/Aβ/NLRP3 pathway was upregulated in DPN patients.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (82473982, 82273930), Major Program of the Natural Science Foundation of the Jiangsu Higher Education Institutions of China (23KJA350002), and the Innovation Projects of State Key Laboratory on Technologies for Chinese Medicine Pharmaceutical Process Control and Intelligent Manufacture (NZYSKL240110).

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  1. These authors contributed equally: Ni-xue Song, Yan-chun Wang, Tong Zhao

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  1. National Key Laboratory on Technologies for Chinese Medicine Pharmaceutical Process Control and Intelligent Manufacture, Nanjing University of Chinese Medicine, Nanjing, 210023, China

    Ni-xue Song, Yan-chun Wang, Tong Zhao, Zhi-shuo Zhang, Jia-cheng Liu, Zi-yun Chen, Yu-jie Huang, Jia-ying Wang & Xu Shen

  2. School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China

    Yu-jie Huang, Jia-ying Wang & Xu Shen

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Contributions

XS, JYW, NXS, YCW and TZ designed the study. XS reviewed the paper. NXS, YCW, TZ, ZSZ, JCL, and ZYC performed the animal and cell experiments. NXS, YCW and TZ analyzed interpreted data. NXS, YJH and JYW wrote the paper. XS, NXS, YCW, TZ, ZSZ, JCL, ZYC, YJH and JYW are the guarantors of this work and, as such, have full access to all data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. All authors approved the paper.

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Song, Nx., Wang, Yc., Zhao, T. et al. Selective inhibition of monoamine oxidase B represents a therapeutic strategy for diabetic peripheral neuropathy. Acta Pharmacol Sin (2026). https://doi.org/10.1038/s41401-026-01764-2

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