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Cancers (Basel). 2024 Feb 15;16(4):789. doi: 10.3390/cancers16040789.
2
CerS6-dependent ceramide synthesis in hypothalamic neurons promotes ER/mitochondrial stress and impairs glucose homeostasis in obese mice.下丘脑神经元中 CerS6 依赖性神经酰胺合成促进内质网/线粒体应激,损害肥胖小鼠的葡萄糖稳态。
Nat Commun. 2023 Nov 29;14(1):7824. doi: 10.1038/s41467-023-42595-7.
3
Faecal metabolome and its determinants in inflammatory bowel disease.炎症性肠病的粪便代谢组及其决定因素。
Gut. 2023 Aug;72(8):1472-1485. doi: 10.1136/gutjnl-2022-328048. Epub 2023 Mar 23.
4
Alkaline sphingomyelinase (NPP7) impacts the homeostasis of intestinal T lymphocyte populations.碱性鞘磷脂酶(NPP7)影响肠道 T 淋巴细胞群体的动态平衡。
Front Immunol. 2023 Jan 19;13:1050625. doi: 10.3389/fimmu.2022.1050625. eCollection 2022.
5
Effects of Milk Polar Lipids on DSS-Induced Colitis Severity Are Dependent on Dietary Fat Content.牛奶极性脂对 DSS 诱导结肠炎严重程度的影响取决于膳食脂肪含量。
Nutrients. 2022 Dec 3;14(23):5145. doi: 10.3390/nu14235145.
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Targeted suppression of human IBD-associated gut microbiota commensals by phage consortia for treatment of intestinal inflammation.靶向抑制人类 IBD 相关肠道微生物共生体的噬菌体组合治疗肠道炎症。
Cell. 2022 Aug 4;185(16):2879-2898.e24. doi: 10.1016/j.cell.2022.07.003.
7
The function of Sphingosine-1-phosphate receptor 2 (S1PR2) in maintaining intestinal barrier and inducing ulcerative colitis.鞘氨醇-1-磷酸受体 2(S1PR2)在维持肠道屏障和诱导溃疡性结肠炎中的作用。
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Host hepatic metabolism is modulated by gut microbiota-derived sphingolipids.肠道微生物衍生的神经酰胺调节宿主肝脏代谢。
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9
S1PR2/RhoA/ROCK1 pathway promotes inflammatory bowel disease by inducing intestinal vascular endothelial barrier damage and M1 macrophage polarization.S1PR2/RhoA/ROCK1 通路通过诱导肠道血管内皮屏障损伤和 M1 巨噬细胞极化促进炎症性肠病。
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Long-chain ceramides are cell non-autonomous signals linking lipotoxicity to endoplasmic reticulum stress in skeletal muscle.长链神经酰胺是一种细胞非自主信号,可将脂肪毒性与骨骼肌内质网应激联系起来。
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鞘脂在炎症性肠病中的多种作用。

The diverse roles of sphingolipids in inflammatory bowel disease.

机构信息

School of Nutritional Sciences and Wellness, University of Arizona, Tucson, Arizona, USA.

University of Arizona Cancer Center, University of Arizona, Tucson, Arizona, USA.

出版信息

FASEB J. 2024 Jul 15;38(13):e23777. doi: 10.1096/fj.202400830R.

DOI:10.1096/fj.202400830R
PMID:38934445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC467036/
Abstract

The incidence of inflammatory bowel disease (IBD) has increased over the last 20 years. A variety of causes, both physiological and environmental, contribute to the initiation and progression of IBD, making disease management challenging. Current treatment options target various aspects of the immune response to dampen intestinal inflammation; however, their effectiveness at retaining remission, their side effects, and loss of response from patients over time warrant further investigation. Finding a common thread within the multitude causes of IBD is critical in developing robust treatment options. Sphingolipids are evolutionary conserved bioactive lipids universally generated in all cell types. This diverse lipid family is involved in a variety of fundamental, yet sometimes opposing, processes such as proliferation and apoptosis. Implicated as regulators in intestinal diseases, sphingolipids are a potential cornerstone in understanding IBD. Herein we will describe the role of host- and microbial-derived sphingolipids as they relate to the many factors of intestinal health and IBD.

摘要

过去 20 年来,炎症性肠病(IBD)的发病率有所上升。多种生理和环境因素导致 IBD 的发生和发展,使得疾病的管理极具挑战性。目前的治疗选择针对免疫反应的多个方面,以抑制肠道炎症;然而,它们在维持缓解、副作用以及随着时间的推移患者的反应丧失方面的有效性需要进一步研究。在 IBD 的众多病因中找到一个共同的线索对于开发强有力的治疗方法至关重要。鞘脂是进化上保守的生物活性脂质,普遍存在于所有细胞类型中。这个多样化的脂质家族参与多种基本但有时相互矛盾的过程,如增殖和凋亡。鞘脂作为肠道疾病的调节因子,是理解 IBD 的一个潜在基石。本文将描述宿主和微生物衍生的鞘脂的作用,因为它们与肠道健康和 IBD 的许多因素有关。