IL-33 promotes pancreatic β-cell survival and insulin secretion under diabetogenic conditions through PPARγ-Reference-Cited by-同舟云学术

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IL-33 promotes pancreatic β-cell survival and insulin secretion under diabetogenic conditions through PPARγ

Published:2023-11 Issue: Volume:959 Page:176059
ISSN:0014-2999
Container-title:European Journal of Pharmacology
language:en
Short-container-title:European Journal of Pharmacology

Author:

Lin Jian,Lan Yan,Xiang Daochun,Ma Rui,Chen Qianjiang,Ding Ke,Lu Jingli^ORCID

Publisher

Elsevier BV

Subject

Pharmacology

Reference39 articles.

1. Lipotoxic endoplasmic reticulum stress, beta cell failure, and type 2 diabetes mellitus;Biden;Trends Endocrinol. Metabol.,2014

2. Mechanisms controlling pancreatic islet cell function in insulin secretion;Campbell;Nat. Rev. Mol. Cell Biol.,2021

3. Interleukin-33-Activated islet-resident innate lymphoid cells promote insulin secretion through myeloid cell retinoic acid production;Dalmas;Immunity,2017

4. Immunological and inflammatory functions of the interleukin-1 family;Dinarello;Annu. Rev. Immunol.,2009

5. IL-33-induced metabolic reprogramming controls the differentiation of alternatively activated macrophages and the resolution of inflammation;Faas;Immunity,2021

Cited by 1 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Whole transcriptome sequencing analyses of islets reveal ncRNA regulatory networks underlying impaired insulin secretion and increased β-cell mass in high fat diet-induced diabetes mellitus;PLOS ONE;2024-04-01

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