Qoreishi Seyedeh Hoda, Khazeei Tabari Mohammad Amin, Găman Mihnea-Alexandru, Kazeminejad Armaghan
Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
USERN Office, Mazandaran University of Medical Sciences, Sari, Iran.
Avicenna J Med Biotechnol. 2024 Jul-Sep;16(3):146-155. doi: 10.18502/ajmb.v16i3.15740.
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.
本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，重点关注分子机制。1型血管紧张素受体（AT1R）在伤口区域大量存在，从而导致ERK、STAT1和STAT3的激活，这可导致表皮自我更新。肾素血管紧张素系统（RAS）成分在烧伤引起的伤口中的表达明显低于完整皮肤，表明RAS参与皮肤的重新上皮化。ERK、STAT和STAT3是血管紧张素II的靶点，表明RAS活性成分参与成纤维细胞、干细胞和角质形成细胞的迁移。抑制RAS对伤口愈合的影响取决于具体情况。一方面，有人认为在此阶段抑制RAS可能会减慢伤口愈合速度。另一方面，研究表明在此阶段抑制RAS可导致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（ARBs）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重要作用。已经表明，抑制RAS可通过下调炎症和纤维化因子，如TGF - β、SMAD2/3、TAK1、PDGF - BB和HSP47来抑制瘢痕形成和纤维化。总之，局部给予RAS调节剂可能会在伤口闭合的最后阶段减少瘢痕形成和炎症。
