4.3 Article

Maltol Promotes Mitophagy and Inhibits Oxidative Stress via the Nrf2/PINK1/Parkin Pathway after Spinal Cord Injury

Journal

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2022, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2022/1337630

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Funding

  1. National Natural Science Foundation of China [81972150, 82172428]
  2. Zhejiang Provincial Natural Science Foundation [LR18H150001, LQ18H090008]

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The study found that maltol can trigger the expression of Nrf2 and promote its retranslocation to the nucleus, thereby obstructing OS signal and apoptosis-mediated neuronal cell death after SCI. Additionally, maltol treatment enhances PINK1/Parkin-mediated mitophagy in PC12 cells, aiding in the recovery of mitochondrial functions. These findings suggest that maltol could be a promising therapeutic candidate for the treatment and management of SCI.
Spinal cord injury (SCI), a fatal disease in the central nervous system, is characteristic of weak neuronal regeneration ability and complex pathological progress. Activation of oxidative stress (OS) and apoptosis-mediated cell death significantly contributes to the progression of SCI. Current evidence suggests that maltol exerts natural antioxidative properties via obstructing OS and apoptosis. However, the significant effect of maltol on SCI treatment has never been evaluated yet. In our current study, we explored maltol administration that could trigger the expression of Nrf2 and promote the retranslocation of Nrf2 from the cytosol to the nucleus, which can subsequently obstruct OS signal and apoptosis-mediated neuronal cell death after SCI. Furthermore, we found that maltol treatment enhances PINK1/Parkin-mediated mitophagy in PC12 cells, facilitating the recovery of mitochondrial functions. Our findings propose that maltol could be a promising therapeutic candidate for the treatment and management of SCI.

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