Sympathetic System in Wound Healing: Multistage Control in Normal and Diabetic Skin
- PMID: 36768369
- PMCID: PMC9916402
- DOI: 10.3390/ijms24032045
Sympathetic System in Wound Healing: Multistage Control in Normal and Diabetic Skin
Abstract
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.
Keywords: NGF; NPY; VIP; acetylcholine; angiogenesis; diabetes mellitus; keratinocytes; norepinephrine; sympathetic system; wound healing.
Conflict of interest statement
The authors declare no conflict of interest.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Molecular Biology Databases
Miscellaneous
