Epigenetic regulation underlying development of chronic pain caused by adipokines

瘦素是一种脂肪因子，可上调巨噬细胞中趋化因子巨噬细胞炎症蛋白(MIP)的表达。周围神经损伤后MIPs表达增加，阻断MIPs信号转导通路可预防神经损伤所致的神经病理性疼痛和神经炎症。此外，组蛋白的过度乙酰化增强了MIPs的表达。总之，脂肪因子在神经病理性疼痛的发展中起着关键作用，伴随着炎症细胞中趋化因子表达的表观遗传增强。

Leptin, an adipokine, up-regulated the chemokine macrophage inflammatory proteins(MIPs) in macrophages. The expression of MIPs was increased in the injured peripheral nerves, and the blockade of MIPs signaling prevented nerve injury-induced neuropathic pain and neuroinflammation. Moreover, MIPs expression was enhanced by the overacetylation of histones. In conclusion, adipokines play key roles in the development of neuropathic pain, accompanied by epigenetic augmentation of chemokine expressions in inflammatory cells.