Vascular nitric oxide resistance in type 2 diabetes.
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
11 07 2023
11 07 2023
Historique:
received:
09
02
2023
accepted:
28
06
2023
revised:
18
06
2023
medline:
13
7
2023
pubmed:
12
7
2023
entrez:
11
7
2023
Statut:
epublish
Résumé
Vascular nitric oxide (NO•) resistance, manifested by an impaired vasodilator function of NO• in both the macro- and microvessels, is a common state in type 2 diabetes (T2D) associated with developing cardiovascular events and death. Here, we summarize experimental and human evidence of vascular NO• resistance in T2D and discuss its underlying mechanisms. Human studies indicate a ~ 13-94% decrease in the endothelium (ET)-dependent vascular smooth muscle (VSM) relaxation and a 6-42% reduced response to NO• donors, i.e., sodium nitroprusside (SNP) and glyceryl trinitrate (GTN), in patients with T2D. A decreased vascular NO• production, NO• inactivation, and impaired responsiveness of VSM to NO• [occurred due to quenching NO• activity, desensitization of its receptor soluble guanylate cyclase (sGC), and/or impairment of its downstream pathway, cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG)] are the known mechanisms underlying the vascular NO• resistance in T2D. Hyperglycemia-induced overproduction of reactive oxygen species (ROS) and vascular insulin resistance are key players in this state. Therefore, upregulating vascular NO• availability, re-sensitizing or bypassing the non-responsive pathways to NO•, and targeting key vascular sources of ROS production may be clinically relevant pharmacological approaches to circumvent T2D-induced vascular NO• resistance.
Identifiants
pubmed: 37433795
doi: 10.1038/s41419-023-05935-5
pii: 10.1038/s41419-023-05935-5
pmc: PMC10336063
doi:
Substances chimiques
Nitric Oxide
31C4KY9ESH
Reactive Oxygen Species
0
Nitric Oxide Donors
0
Cyclic GMP
H2D2X058MU
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
410Informations de copyright
© 2023. The Author(s).
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