Age-dependent decline in remyelination capacity is mediated by apelin–APJ signaling

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Abstract

Age-related regeneration failure in the central nervous system can occur as a result of a decline in remyelination efficacy. The responsiveness of myelin-forming cells to signals for remyelination is affected by aging-related epigenetic modification; however, the molecular mechanism is not fully clarified. In the present study, we report that the apelin receptor (APJ) mediates remyelination efficiency with age. APJ expression in myelin-forming cells is correlated with age-associated changes in remyelination efficiency, and the activation of APJ promotes remyelination through the translocation of myelin regulatory factor. APJ signaling activation promoted remyelination in both aged mice with toxin-induced demyelination and mice with experimental autoimmune encephalomyelitis. In human cells, APJ activation enhanced the expression of remyelination markers. Impaired oligodendrocyte function in aged animals can be reversibly reactivated; thus, the results demonstrate that dysfunction of the apelin–APJ system mediates remyelination failure in aged animals, and that their myelinating function can be reactivated by APJ activation.

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Ito, M., Muramatsu, R., Kato, Y., Sharma, B., Uyeda, A., Tanabe, S., … Yamashita, T. (2021). Age-dependent decline in remyelination capacity is mediated by apelin–APJ signaling. Nature Aging, 1(3), 284–294. https://doi.org/10.1038/s43587-021-00041-7

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