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更新于：2025-01-23

Sphingomyelin

更新于：2025-01-23

基本信息

别名

鞘磷脂类

简介-

关联

项与 Sphingomyelin 相关的药物

BF/PC-13

靶点

Sphingomyelin

作用机制

Sphingomyelin抑制剂

在研机构-

原研机构

Biofrontera Bioscience GmbH

在研适应症-

非在研适应症

皮炎 [+1]

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 Sphingomyelin 相关的临床结果

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100 项与 Sphingomyelin 相关的转化医学

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0 项与 Sphingomyelin 相关的专利（医药）

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399

项与 Sphingomyelin 相关的文献（医药）

2025-02-01·Journal of Stroke and Cerebrovascular Diseases

Mendelian randomization and mediation examination of the immune cell-mediated link between sphingomyelin and stroke

Article

作者: Wang, Guangming ; Xu, Yonghong ; Xu, Cong ; Ma, Jianglei

OBJECTIVEThe study established a direct link between stroke and sphingomyelin. The precise biology underlying this connection is yet unknown, though. As a result, we decided to investigate the potential causal relationship between Sphingomyelin and genetic vulnerability to stroke, as well as the potential mediating function that immune cells may play in this process, using Mendelian randomization (MR) approaches.METHODSA published genome-wide association study (GWAS) dataset of European populations served as the foundation for the MR Study. The inverse variance weighting (IVW) model is the main technique. Four additional statistical techniques (MR Egger, Weighted median, Simple mode, and Weighted mode) were also employed to enhance the verification process. Reverse MR Analysis was utilized to reinforce the findings, and heterogeneity and horizontal pleipotency were assessed. Additionally, this study looked into potential immune cell mediating roles in the causal link between sphingomyelin and stroke using two-step MR techniques.RESULTThe IVW metod's results indicated that sphingomyelin genetic susceptibility was linked to a high risk of stroke (OR = 1.045 [95 %CI, 1.004-1.087; P = 0.031). Additionally, the statistical result of SSC-A on CD8br and stroke was IVW [P = 0.007, OR(95 % CI) 1.020 (1.005-1.034)], which was proportionate to the increased risk of stroke. A lower incidence of stroke IVW is linked to CD45 on CD8br [P = 0.004, OR(95 % CI) 0.993 (0.988-0.998)]. Furthermore, our results imply that SSC-A on CD8br and CD45 on CD8br contribute to the causative relationship between sphingomyelin and stroke. The percentages of conciliation are 5.38 %, 22.7 %, 33.5 %), and 0.000999, 0.0152, 0.0132, respectively.CONCLUSIONWe confirmed the effect of sphingomyelin on stroke and conducted in-depth studies. SSC-A on CD8br and CD45 on CD8br is latent stroke mediators associated with sphingomyelin. Through two-step mediated Mendelian randomization analysis, we provide new insights into the etiology and treatment of stroke.

2025-02-01·Food Chemistry

Size-dependent composition and in-situ structure analysis of the milk fat globule membrane in buffalo milk

Article

作者: Zhang, Weibo ; Yu, Jinghua ; Ren, Fazheng ; Wu, Shouyun ; Wu, Peipei ; Wang, Yi ; Wei, Jianhuan ; Wang, Pengjie ; Luo, Jie ; Chen, Chong ; Guo, Mengyuan

This study provides insights into the composition and in-situ structures of the milk fat globule membrane (MFGM) in buffalo milk with different fat globule sizes (0.55 μm and 8.04 μm). Small fat globules contained a higher amount of MFGM proteins and polar lipids, while the content of MFGM components (except for ADPH) was greater per unit membrane area in large fat globules. A total of 386 differentially expressed proteins were identified, with many of the most differentially expressed proteins being associated with human diseases, such as cancer and elderly diseases. The coverage of sphingomyelin and certain MFGM proteins (BTN and PAS 6/7) on large fat globules was higher, potentially linked to the presence of larger, irregular lipid rafts and patch-shaped glycocalyxes, respectively. These findings suggest that small fat globules are suitable for nutritional fortification of buffalo milk, while large fat globules are appropriate for the preparation of functional dairy-based ingredients.

2025-01-01·Ophthalmology Science

Interplay between Lipids and Complement Proteins—How Multiomics Data Integration Can Help Unravel Age-related Macular Degeneration Pathophysiology: A Proof-of-concept Study

Article

作者: Wong, Tien Yin ; Cheung, Danny ; Tham, Yih Chung ; Cheung, Chui Ming Gemmy ; Wang, Xiaomeng ; Nusinovici, Simon ; Chakravarthy, Usha ; Gemmy Cheung, Chui Ming ; Li, Hengtong ; Cheng, Ching-Yu ; Raghavan, Lavanya ; Zhou, Lei

ObjectiveOur objectives were to identify correlation patterns between complement and lipid pathways using a multiomics data integration approach and to determine how these interconnections affect age-related macular degeneration (AMD).DesignNested case-control study.Subjects and ControlsThe analyses were performed in a subset of the Singapore Indian Eye Study. We randomly selected 155 AMD cases and age- and sex-matched them with 155 controls.MethodsFirstly, a multiomics data integration method was used to identify correlation patterns between the omics data. Then, we tested possible interactions between the lipids and complement proteins using logistic regression models.Main Outcome MeasuresAge-related macular degeneration was determined according to the Beckman classification system. We measured in serum samples 35 complement proteins and 66 lipids, and used 9 genetic variants.ResultsAmong the 155 AMD cases, 93 (60.0%) had early and 62 (40.0%) intermediate AMD. Firstly, we identified 2 clusters between complement proteins and lipids involving (1) mannan-binding lectin serine protease 1 and several different high-density lipoprotein particles, and (2) complement factor H-related protein 1, carboxypeptidase N subunit 2 and complement component C8 gamma chain, and sphingomyelin and different cholesterol. Secondly, we identified 1 interaction between complement protein 1R and sphingomyelin with an odds of AMD 2 times higher for individuals with low levels of sphingomyelin and complement protein 1R (odds ratio = 2.13 [1.09, 4.17]).ConclusionsWe report here, using a cutting-edge multiomics integration approach, the complex interconnections between genetic, metabolomics, and proteomic data. This method permitted us to obtain a holistic picture and identify multiomics signature of AMD pathophysiology. These results advocate for a personalized therapeutic approach that accounts for multiple pathways. However, these results need to be validated in larger studies with different ethnic groups.Financial DisclosuresProprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

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