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首页> 外文期刊>The Journal of investigative dermatology. >When Beauty Is Skin Deep: Regulation of the Wound Response by Caspase-8, RIPK3, and the Inflammasome
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When Beauty Is Skin Deep: Regulation of the Wound Response by Caspase-8, RIPK3, and the Inflammasome

机译：当美丽深处时：Caspase-8，RIPK3和炎症小体对伤口反应的调节

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Caspase-8 downregulation is observed in the epidermis of wounded skin, whereas permanent epidermal caspase-8 deletion causes chronic skin inflammation, suggesting that caspase-8 is a critical regulator of skin homeostasis and, possibly, the wound response. In this issue, Lee et al. document how epidermal caspase-8 deletion, or cutaneous wounding, results in increased NE-kappa B activation to drive keratinocyte caspase-1 expression and subsequent secretion of the proinflammatory cytokines, IL-1 beta and IL-1 alpha. Consequently, loss of NF-kappa B activity, caspase-1, or the IL-1 receptor delays wound healing. Previous studies have documented how chronic skin inflammation in caspase-8-deficient mice is rescued by RIPK3 co-deletion. Therefore, targeting caspase-1, IL-1, or RIPK3 itself may benefit treatment of chronic inflammatory skin diseases, or where an inappropriate inflammatory response proves detrimental to wound healing, such as in type 2 diabetes.
机译：在受伤皮肤的表皮中观察到caspase-8的下调，而永久性表皮caspase-8缺失会引起慢性皮肤炎症，这表明caspase-8是皮肤稳态和可能的伤口反应的关键调节剂。在这个问题上，李等人。文献记载了表皮caspase-8缺失或皮肤受伤如何导致NE-κB活化增加以驱动角质形成细胞caspase-1表达，并随后分泌促炎性细胞因子IL-1β和IL-1α。因此，NF-κB活性，caspase-1或IL-1受体的丧失会延迟伤口的愈合。先前的研究已记录了如何通过RIPK3共缺失挽救caspase-8缺陷型小鼠的慢性皮肤炎症。因此，靶向caspase-1，IL-1或RIPK3本身可能有益于慢性炎症性皮肤病的治疗，或不适当地的炎症反应证明对伤口愈合不利的疾病，例如2型糖尿病。

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