抄録
Diabetes mellitus is one of the major risk factors for cardiovascular disease and is an important health issue worldwide. Long-term diabetes causes endothelial dysfunction, which in turn leads to diabetic vascular complications. Endothelium-derived nitric oxide is a major vasodilator in large-size vessels, and the hyperpolarization of vascular smooth muscle cells mediated by the endothelium plays a central role in agonist-mediated and flow-mediated vasodilation in resistance-size vessels. Although the mechanisms underlying diabetic vascular complications are multifactorial and complex, impairment of endothelium-dependent hyperpolarization (EDH) of vascular smooth muscle cells would contribute at least partly to the initiation and progression of microvascular complications of diabetes. In this review, we present the current knowledge about the pathophysiology and underlying mechanisms of impaired EDH in diabetes in animals and humans. We also discuss potential therapeutic approaches aimed at the prevention and restoration of EDH in diabetes.
| 元の言語 | 英語 |
|---|---|
| 記事番号 | 3737 |
| ジャーナル | International journal of molecular sciences |
| 巻 | 20 |
| 発行部数 | 15 |
| DOI | |
| 出版物ステータス | 出版済み - 8 1 2019 |
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All Science Journal Classification (ASJC) codes
- Catalysis
- Molecular Biology
- Spectroscopy
- Computer Science Applications
- Physical and Theoretical Chemistry
- Organic Chemistry
- Inorganic Chemistry
これを引用
Endothelium-dependent hyperpolarization (EDH) in diabetes : Mechanistic insights and therapeutic implications. / Goto, Kenichi; Kitazono, Takanari.
：: International journal of molecular sciences, 巻 20, 番号 15, 3737, 01.08.2019.研究成果: ジャーナルへの寄稿 › 評論記事
}
TY - JOUR
T1 - Endothelium-dependent hyperpolarization (EDH) in diabetes
T2 - Mechanistic insights and therapeutic implications
AU - Goto, Kenichi
AU - Kitazono, Takanari
PY - 2019/8/1
Y1 - 2019/8/1
N2 - Diabetes mellitus is one of the major risk factors for cardiovascular disease and is an important health issue worldwide. Long-term diabetes causes endothelial dysfunction, which in turn leads to diabetic vascular complications. Endothelium-derived nitric oxide is a major vasodilator in large-size vessels, and the hyperpolarization of vascular smooth muscle cells mediated by the endothelium plays a central role in agonist-mediated and flow-mediated vasodilation in resistance-size vessels. Although the mechanisms underlying diabetic vascular complications are multifactorial and complex, impairment of endothelium-dependent hyperpolarization (EDH) of vascular smooth muscle cells would contribute at least partly to the initiation and progression of microvascular complications of diabetes. In this review, we present the current knowledge about the pathophysiology and underlying mechanisms of impaired EDH in diabetes in animals and humans. We also discuss potential therapeutic approaches aimed at the prevention and restoration of EDH in diabetes.
AB - Diabetes mellitus is one of the major risk factors for cardiovascular disease and is an important health issue worldwide. Long-term diabetes causes endothelial dysfunction, which in turn leads to diabetic vascular complications. Endothelium-derived nitric oxide is a major vasodilator in large-size vessels, and the hyperpolarization of vascular smooth muscle cells mediated by the endothelium plays a central role in agonist-mediated and flow-mediated vasodilation in resistance-size vessels. Although the mechanisms underlying diabetic vascular complications are multifactorial and complex, impairment of endothelium-dependent hyperpolarization (EDH) of vascular smooth muscle cells would contribute at least partly to the initiation and progression of microvascular complications of diabetes. In this review, we present the current knowledge about the pathophysiology and underlying mechanisms of impaired EDH in diabetes in animals and humans. We also discuss potential therapeutic approaches aimed at the prevention and restoration of EDH in diabetes.
UR - http://www.scopus.com/inward/record.url?scp=85070557363&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85070557363&partnerID=8YFLogxK
U2 - 10.3390/ijms20153737
DO - 10.3390/ijms20153737
M3 - Review article
C2 - 31370156
AN - SCOPUS:85070557363
VL - 20
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
SN - 1661-6596
IS - 15
M1 - 3737
ER -