Mechanisms Underlying UC-MSC-Mediated Suppression of Thyroid EMT (PRJCA039436)
收藏NIAID Data Ecosystem2026-05-10 收录
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资源简介：
Thyroid Organoid Model Unveils Mesenchymal Stem Cell Mediated EMT Antagonism in Suppressing Fibrosis of Hashimoto's Thyroiditis
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创建时间：
2025-11-20
相关数据集
附表1-15.xlsx
题目：血清脂质和降脂药物靶基因对自身免疫性甲状腺疾病的因果影响的遗传学见解. 抽象 背景：血清脂质或降脂药物在AITD患者中的作用仍然 令人困惑。目的： 的 脂 质性状、降脂药物靶基因与AITD方法：采用孟德尔随机化（MR）分析，评估脂质性状以及10个降脂药物靶基因对AITD的影响。欧洲血统的 AITD 汇总统计数据来自 FinnGen R10，包括 Graves 病 （G
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Distribution of haplotypes frequencies for CTLA4 gene polymorphisms (+49A/G and CT60A/G) among autoimmune hypothyroidism patients and controls.
Distribution of haplotypes frequencies for CTLA4 gene polymorphisms (+49A/G and CT60A/G) among autoimmune hypothyroidism patients and controls.
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ACOT1, ACOT2, and ACOT3 are involved in fatty acid metabolism and Cyp4a10, and Cyp4a14 are involved in the PPAR signaling pathway downregulated significantly after MSCs treatment in WD-induced NASH liver.. ACOT1, ACOT2, and ACOT3 are involved in fatty acid metabolism and Cyp4a10, and Cyp4a14 are involved in the PPAR signaling pathway downregulated significantly after MSCs treatment in WD-induced NASH liver.
To identify the therapeutic role of hUC-MSCs cell therapy in WD-induced NASH, we established a NASH mouse model. Overall design: We evaluated the therapeutic efficacy of human umbilical cord-derived M
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Human umbilical cord blood-derived MSCs trans-differentiate into endometrial cells and regulate Th17/Treg balance through NF-B signaling in rabbit intrauterine adhesions endometrium [RNA-seq]
Purpose: The fundamental cause of intrauterine adhesions (IUAs) is the destruction and reduction of stem cells in endometrial basal layer, resulting in endometrial reconstruction very difficult. The p
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Intratracheal transplantation of mesenchymal stem cells attenuates hyperoxia-induced lung injury by down-regulating, but not direct inhibiting formyl peptide receptor 1 in the newborn mice
Formyl peptide receptor 1 (FPR1) has been shown to be a key regulator of inflammation. However, its role in bronchopulmonary dysplasia (BPD) has not been delineated yet. We investigated whether FPR1 p
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