期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-03943-0
关键词
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资金
- Juvenile Diabetes Research Foundation [17-2013-372, 3-RSC-2016-162-I-X]
- Consejeria de Salud, Fundacion Publica Andaluza Progreso y Salud, Junta de Andalucia [PI-0727-2010, P10CTS6505]
- Consejeria de Economia, Innovacion y Ciencia [P10.CTS.6359]
- Ministerio de Economia y Competidividad
- Fondos FEDER [PI10/00871, PI13/00593, BFU2017-83588-P, PI14/01015, RD12/0019/0028, RD16/0011/0034, PI16/00259]
- Deutsche Forschungsgemeinschaft [GRK-1789, DFG SCHI-505/6-1]
- DiabetesCero Foundation
- Instituto de Salud Carlos III [CP14/00105]
- Fondos FEDER
- Juan de la Cierva Fellowship
- Amarna Therapeutics
Type 1 diabetes mellitus (T1DM) is due to the selective destruction of islet beta cells by immune cells. Current therapies focused on repressing the immune attack or stimulating beta cell regeneration still have limited clinical efficacy. Therefore, it is timely to identify innovative targets to dampen the immune process, while promoting beta cell survival and function. Liver receptor homologue-1 (LRH-1) is a nuclear receptor that represses inflammation in digestive organs, and protects pancreatic islets against apoptosis. Here, we show that BL001, a small LRH-1 agonist, impedes hyperglycemia progression and the immune-dependent inflammation of pancreas in murine models of T1DM, and beta cell apoptosis in islets of type 2 diabetic patients, while increasing beta cell mass and insulin secretion. Thus, we suggest that LRH-1 agonism favors a dialogue between immune and islet cells, which could be druggable to protect against diabetes mellitus.
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