HMGB1:诱导RIRI早期的内源性危险信号?

The High Mobility Group Box 1(HMGB1)is an Endogenous Risk Signal that Could Induce the Early Period Inflammatory of Renal Ischemia-reperfusion Injury(RIRI)?

肾脏缺血时,坏死和凋亡的肾小管上皮及血管内皮细胞会释放出高迁移率族蛋白(high mobility group box 1,HMGB1)。HMGB1可能是诱导肾脏缺血再灌注损伤(renal ischemia and reperfusion injury,RIRI)早期的内源性危险信号。本研究主要阐述了在RIRI早期胞外HMGB1的来源以及与RIRI的关系。HMGB1可促使天然调节型T细胞(nTreg)丧失炎症抑制作用甚至可能翻转为促炎性细胞,该分子同时诱导巨噬细胞分泌大量炎性因子,并作用于活化的巨噬细胞使其自分泌HMGB1,二者共同作用造成肾脏缺血再灌注早期炎症损伤。如在损伤早期阻断HMGB1的多重作用,不仅可以消除巨噬细胞的炎症反应,而且可能恢复nTreg的炎症抑制作用从而减轻炎症反应,可能会对肾脏起到更好的保护作用。

HMGB1 can be released from necrotic and apoptotic renal tubular epithelial and endothelial cells in renal ischemia.HMGB1 may be an endogenous danger signal to induce the inflammatory in the eraly renal ischemia and reperfusion injury(RIRI).In this review,we focued on the source of extracellular HMGB1,the relationship between HMGB1 and RIRI.HMGB1 could promote the loss of suppression function of the Natural Regulatory T Cells(nTreg)and even may reverse to pro-inflammatory cells.HMGB1 may induce macrophage to secrete a large number of inflammatory cytokines and act on activated macrophages to autocrine HMGB1.They cause inflammatory damage in the early RIRI.If blocking the multiple effects of HMGB1,in the eraly RIRI,could not only eliminate the inflammatory response of macrophages,but also restore the suppression function of nTreg,thereby reducing the inflammatory response,which may play a better protective role on the kidney.