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摘要: 糖尿病创面是糖尿病并发症,其难以愈合,易转为慢性创面。与普通创面愈合相比,糖尿病创面停留在炎症期,无法进入增殖期,原因为促炎性细胞因子比例增加造成炎症细胞比例失调,大量炎症因子堆积。炎症因子的产生、释放与细胞焦亡密切相关。细胞焦亡是一种炎症细胞程序性死亡方式。在炎症小体介导下,细胞焦亡通过典型与非典型炎症小体信号通路转导,造成细胞膜上形成孔隙,诱发细胞死亡,并在此过程中释放大量促炎性细胞因子,维持创面的炎症环境,阻碍糖尿病创面向增殖期、重塑期发展,从而抑制糖尿病创面愈合。该文就细胞焦亡机制及细胞焦亡对糖尿病创面的影响、抑制细胞焦亡在糖尿病创面治疗中的潜在意义以及存在的相关问题进行综述。Abstract: Diabetic wound is a complication of diabetes, which is difficult to heal and easy to turn into chronic wound. Compared with ordinary wound healing, diabetic wounds stay in the inflammatory stage and can not enter the proliferative stage. This is because the proportion of pro-inflammatory cytokines increases, leading to the imbalance of inflammatory cells and the accumulation of a large number of inflammatory factors. The production and release of inflammatory factors is closely related to pyroptosis. Pyroptosis is a kind of programmed death mode of inflammatory cells. Mediated by inflammasome, pyroptosis is transduced through typical and atypical inflammasome signaling pathways, resulting in the formation of pores on the cell membrane and inducing cell death. In this process, a large number of pro-inflammatory cytokines are released to maintain the inflammatory environment of wounds, hindering the development of diabetic wounds to the proliferative stage and remodeling stage, thus inhibiting the healing of diabetic wounds. This article reviews the mechanism of pyroptosis and its effect on diabetic wounds, the potential significance of inhibiting pyroptosis in the treatment of diabetic wounds, and the existing problems.
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Key words:
- Pyroptosis /
- Inflammation /
- Cytokines /
- Diabetes complications /
- Wound healing /
- Inflammasome
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参考文献
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图 1 炎症期糖尿病创面中细胞焦亡的作用机制
注：IL为白细胞介素,pro-IL为IL前体,NLRP3为核苷酸结合寡聚化结构域样受体蛋白3,caspase为胱天蛋白酶,pro-caspase为caspase前体,TXNIP为硫氧还蛋白相互作用蛋白；图中黑色箭头表示促进,蓝色箭头表示剪切,绿色箭头表示寡聚化
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