Faculty of Medicine, Lomonosov Moscow State University, 119991 Moscow, Russia.
Int J Mol Sci. 2023 Jan 20;24(3):2045. doi: 10.3390/ijms24032045.
In this review, we discuss sympathetic regulation in normal and diabetic wound healing. Experimental denervation studies have confirmed that sympathetic nerve endings in skin have an important and complex role in wound healing. Vasoconstrictor neurons secrete norepinephrine (NE) and neuropeptide Y (NPY). Both mediators decrease blood flow and interact with inflammatory cells and keratinocytes. NE acts in an ambiguous way depending on receptor type. Beta2-adrenoceptors could be activated near sympathetic endings; they suppress inflammation and re-epithelialization. Alpha1- and alpha2-adrenoceptors induce inflammation and activate keratinocytes. Sudomotor neurons secrete acetylcholine (ACh) and vasoactive intestinal peptide (VIP). Both induce vasodilatation, angiogenesis, inflammation, keratinocytes proliferation and migration. In healthy skin, all effects are important for successful healing. In treatment of diabetic ulcers, mediator balance could be shifted in different ways. Beta2-adrenoceptors blockade and nicotinic ACh receptors activation are the most promising directions in treatment of diabetic ulcers with neuropathy, but they require further research.
在这篇综述中，我们讨论了正常和糖尿病伤口愈合中的交感调节。实验性去神经研究证实，皮肤中的交感神经末梢在伤口愈合中具有重要而复杂的作用。血管收缩神经元分泌去甲肾上腺素（NE）和神经肽 Y（NPY）。这两种介质都可减少血流量，并与炎症细胞和角质形成细胞相互作用。NE 根据受体类型而表现出模糊的作用。β2-肾上腺素能受体可在交感神经末梢附近被激活；它们可抑制炎症和再上皮化。α1-和α2-肾上腺素能受体可引发炎症并激活角质形成细胞。汗腺神经元分泌乙酰胆碱（ACh）和血管活性肠肽（VIP）。两者均可引起血管扩张、血管生成、炎症、角质形成细胞增殖和迁移。在健康皮肤中，所有这些作用对于成功愈合都很重要。在治疗糖尿病性溃疡时，介质平衡可能会以不同的方式发生偏移。β2-肾上腺素能受体阻断和烟碱型乙酰胆碱受体激活是治疗伴有神经病变的糖尿病性溃疡最有前途的方向，但仍需要进一步研究。
