Nitric Oxide Synthases in Rheumatoid Arthritis.
disease-modifying antirheumatic drugs
inflammatory cytokines
nitric oxide
nitric oxide synthases
rheumatoid arthritis
Journal
Molecules (Basel, Switzerland)
ISSN: 1420-3049
Titre abrégé: Molecules
Pays: Switzerland
ID NLM: 100964009
Informations de publication
Date de publication:
29 May 2023
29 May 2023
Historique:
received:
19
04
2023
revised:
15
05
2023
accepted:
24
05
2023
medline:
12
6
2023
pubmed:
10
6
2023
entrez:
10
6
2023
Statut:
epublish
Résumé
Rheumatoid arthritis (RA) is an autoimmune disease characterized by severe joint damage and disability. However, the specific mechanism of RA has not been thoroughly clarified over the past decade. Nitric oxide (NO), a kind of gas messenger molecule with many molecular targets, is demonstrated to have significant roles in histopathology and homeostasis. Three nitric oxide synthases (NOS) are related to producing NO and regulating the generation of NO. Based on the latest studies, NOS/NO signaling pathways play a key role in the pathogenesis of RA. Overproduction of NO can induce the generation and release of inflammatory cytokines and act as free radical gas to accumulate and trigger oxidative stress, which can involve in the pathogenesis of RA. Therefore, targeting NOS and its upstream and downstream signaling pathways may be an effective approach to managing RA. This review clearly summarizes the NOS/NO signaling pathway, the pathological changes of RA, the involvement of NOS/NO in RA pathogenesis and the conventional and novel drugs based on NOS/NO signaling pathways that are still in clinical trials and have good therapeutic potential in recent years, with an aim to provide a theoretical basis for further exploration of the role of NOS/NO in the pathogenesis, prevention and treatment of RA.
Identifiants
pubmed: 37298893
pii: molecules28114414
doi: 10.3390/molecules28114414
pmc: PMC10254167
pii:
doi:
Substances chimiques
Nitric Oxide
31C4KY9ESH
Nitric Oxide Synthase
EC 1.14.13.39
Free Radicals
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Natural Science Foundation of China
ID : 82060661, 81660751, 81660151
Organisme : Jiangxi Provincial Natural Science Foundation of China
ID : 20212BAB206092
Organisme : Educational Commission of Jiangxi Province of China
ID : GJJ218104
Organisme : Teaching reform research project of Jiangxi Province of China
ID : JXJG-22-130-1
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