这项研究的目的是回顾肾素-血管紧张素在皮肤再生和伤口愈合中的作用,重点是分子机制。血管紧张素受体1型(AT1R)在伤区丰富,因此,导致ERK的激活,STAT1和STAT3可导致表皮自我更新。灼伤所致创面中肾素血管紧张素系统(RAS)成分的表达明显降低,而不是完整的皮肤,注意RAS参与皮肤的再上皮化。ERK,STAT和STAT3是AngII的目标,表明RAS活性成分参与成纤维细胞,干细胞和角质形成细胞迁移。抑制RAS对伤口愈合的作用是环境依赖性的。一方面,建议在此阶段抑制RAS可能会减慢伤口愈合速度。另一方面,研究表明,在这一阶段抑制RAS可以导致α-SMA激活,最终加速伤口愈合过程。大多数研究表明,用血管紧张素受体阻滞剂(ARB)和血管紧张素转换酶(ACE)抑制RAS在伤口愈合的最后阶段的组织重塑中起着重要作用。已经表明,抑制RAS可以通过下调炎症和纤维化因子来抑制瘢痕形成和纤维化,如TGF-β,SMAD2/3和TAK1、PDGF-BB,HSP47总而言之,在伤口闭合的最后阶段,局部施用RAS调节剂可能导致更少的疤痕形成和炎症。
The aim of this study is to review the role of renin-
angiotensin in skin regeneration and wound healing with a focus on molecular mechanisms.
Angiotensin receptor type 1 (AT1R) are abundant in the wounded area, and thus, lead to the activation of ERK, STAT1, and STAT3 which can lead to epidermal self-renewal. The expression of Renin
Angiotensin System (RAS) components was significantly lower in wounds caused by burning, rather than intact skin, noting that RAS is involved in the re-epithelialization of skin. ERK, STAT and STAT3 are the targets of Ang II, indicating that RAS active components are involved in fibroblast, stem cells and keratinocyte migration. The effect of inhibiting the RAS on wound healing is context-dependent. On one hand, it is suggested that inhibiting RAS during this phase may slow down wound healing speed. On the other hand, studies have shown that RAS inhibition in this phase can lead to α-SMA activation, ultimately accelerating the wound healing process. Most of the investigations indicate that the inhibition of RAS with
Angiotensin Receptor Blockers (ARBs) and
Angiotensin Converting Enzyme (ACE) plays a significant role in tissue remodeling in the last phase of wound healing. It has been shown that the inhibition of RAS can inhibit scar formation and fibrosis through the downregulation of inflammatory and fibrogenic agents, such as TGF-β, SMAD2/3, and TAK1, PDGF-BB, and HSP47. To sum up, that local administration of RAS regulators might lead to less scar formation and inflammation in the last phase of wound closure.