Departamento de Ciencias Básicas and Center of Molecular Biology and Pharmacogenetics, Universidad de La Frontera, Temuco, Chile.
Laboratorio de Patologia Celular, Instituto de Anatomia, Histologia y Patologia, Universidad Austral de Chile, Valdivia, Chile.
Yale J Biol Med. 2020 Mar 27;93(1):175-185. eCollection 2020 Mar.
Kinins are proinflammatory peptides that are formed in the skin by the enzymatic action of tissue kallikrein (KLK1) on kininogens. Tissue kallikrein is produced by eccrine sweat glands and also by cells of the and other skin appendages. Kinin formation may be favored during inflammatory skin disorders when plasma constituents, including kininogens, extravasate from venules and capillaries, which have increased permeability in response to the plethora of inflammatory mediators generated in the course of acute inflammation. By activating either kinin B1 or B2 receptors, kinins modulate keratinocyte differentiation, which relays on activation of several signaling systems that follows receptor stimulation. Participation of the kinin B1 receptor in wound healing is still a matter of controversy though some studies indicate that B1 receptor stimulation regulates keratinocyte migration by controlling metalloproteases 2 and 9 production and by improving wound closure in a mouse model. Development of more stable kinin B1 receptor agonists may be beneficial to modulate wound healing, especially if we take into account that the B1 receptor is up-regulated by inflammation and by cytokines generated in the inflamed microenvironment.
激肽是一种促炎肽，在皮肤中由组织激肽释放酶（KLK1）对激肽原的酶促作用形成。组织激肽由汗腺和 以及其他皮肤附属物的细胞产生。在炎症性皮肤疾病中，当包括激肽原在内的血浆成分从小静脉和毛细血管渗出时，激肽的形成可能会受到青睐，因为这些血管的通透性增加是对急性炎症过程中产生的大量炎症介质的反应。通过激活激肽 B1 或 B2 受体，激肽调节角质形成细胞分化，这依赖于受体刺激后激活的几个信号系统。尽管一些研究表明 B1 受体刺激通过控制金属蛋白酶 2 和 9 的产生和改善小鼠模型中的伤口闭合来调节角质形成细胞迁移，但激肽 B1 受体参与伤口愈合仍然存在争议。开发更稳定的激肽 B1 受体激动剂可能有助于调节伤口愈合，特别是如果我们考虑到 B1 受体被炎症和炎症微环境中产生的细胞因子上调。
