Vascular Endothelial Growth Factor as an Immediate-Early Activator of Ultraviolet-Induced Skin Injury.
Journal
Mayo Clinic proceedings
ISSN: 1942-5546
Titre abrégé: Mayo Clin Proc
Pays: England
ID NLM: 0405543
Informations de publication
Date de publication:
01 2022
01 2022
Historique:
received:
28
08
2020
revised:
16
07
2021
accepted:
25
08
2021
pubmed:
27
11
2021
medline:
10
2
2022
entrez:
26
11
2021
Statut:
ppublish
Résumé
The negative health consequences of acute ultraviolet (UV) exposure are evident, with reports of 30,000 emergency room visits annually to treat the effects of sunburn in the United States alone. The acute effects of sunburn include erythema, edema, severe pain, and chronic overexposure to UV radiation, leading to skin cancer. Whereas the pain associated with the acute effects of sunburn may be relieved by current interventions, existing post-sunburn treatments are not capable of reversing the cumulative and long-term pathological effects of UV exposure, an unmet clinical need. Here we show that activation of the vascular endothelial growth factor (VEGF) pathway is a direct and immediate consequence of acute UV exposure, and activation of VEGF signaling is necessary for initiating the acute pathological effects of sunburn. In UV-exposed human subjects, VEGF signaling is activated within hours. Topical delivery of VEGF pathway inhibitors, targeted against the ligand VEGF-A (gold nanoparticles conjugated with anti-VEGF antibodies) and small-molecule antagonists of VEGF receptor signaling, prevent the development of erythema and edema in UV-exposed mice. These findings collectively suggest targeting VEGF signaling may reduce the subsequent inflammation and pathology associated with UV-induced skin damage, revealing a new postexposure therapeutic window to potentially inhibit the known detrimental effects of UV on human skin. It is essential to emphasize that these preclinical studies must not be construed as suggesting in any way the use of VEGF inhibitors as a sunburn treatment in humans because warranted future clinical studies and appropriate agency approval are essential in that regard.
Identifiants
pubmed: 34823856
pii: S0025-6196(21)00643-1
doi: 10.1016/j.mayocp.2021.08.018
pmc: PMC8742788
mid: NIHMS1761457
pii:
doi:
Substances chimiques
Vascular Endothelial Growth Factor A
0
Vascular Endothelial Growth Factor Receptor-2
EC 2.7.10.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
154-164Subventions
Organisme : NCI NIH HHS
ID : R01 CA260449
Pays : United States
Organisme : NCI NIH HHS
ID : R29 CA078383
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA015083
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM063904
Pays : United States
Organisme : NIGMS NIH HHS
ID : R56 GM063904
Pays : United States
Organisme : NCI NIH HHS
ID : K99 CA187035
Pays : United States
Organisme : NCI NIH HHS
ID : K08 CA215105
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA150190
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA078383
Pays : United States
Organisme : NCI NIH HHS
ID : R00 CA187035
Pays : United States
Organisme : NIDDK NIH HHS
ID : F30 DK083219
Pays : United States
Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
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