Pharmacological blockade of the EP3 prostaglandin E<sub>2</sub> receptor in the setting of type 2 diabetes enhances β-cell proliferation and identity and relieves oxidative damage.
第一作者:
Karin J,Bosma
第一单位:
Dept. of Veterans Affairs Tennessee Valley Authority, Nashville, TN, USA; Dept. of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
作者:
主题词
动物(Animals);细胞增殖(Cell Proliferation);糖尿病, 2型(Diabetes Mellitus, Type 2);胰岛素分泌细胞(Insulin-Secreting Cells);男(雄)性(Male);小鼠(Mice);小鼠, 近交C57BL(Mice, Inbred C57BL);小鼠, 肥胖(Mice, Obese);氧化性应激(Oxidative Stress);受体, 前列腺素E, EP3亚型(Receptors, Prostaglandin E, EP3 Subtype)
DOI
10.1016/j.molmet.2021.101347
PMID
34626853
发布时间
2024-10-24
- 浏览0
Molecular metabolism
2021年54卷
101347页
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