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Last update 23 Jan 2025

LY86

Last update 23 Jan 2025

Basic Info

Synonyms

dJ80N2.1, Ly-86, LY86

+ [4]

Introduction

May cooperate with CD180 and TLR4 to mediate the innate immune response to bacterial lipopolysaccharide (LPS) and cytokine production. Important for efficient CD180 cell surface expression (By similarity).

Drugs associated with LY86

AAV8-MD1 gene therapy (Genethon)

Target

LY86

Mechanism

LY86 inhibitors [+1]

Active Org.-

Originator Org.

Genethon

Active Indication-

Inactive Indication

Muscular Dystrophy, Duchenne

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with LY86

100 Translational Medicine associated with LY86

0 Patents (Medical) associated with LY86

233

Literatures (Medical) associated with LY86

01 Dec 2024·JACC: Case Reports

Managing Myotonic Dystrophy Type 1 Complicated by Metabolic Syndrome

Article

Author: Pagnoni, Gianluca ; Paolini, Matteo ; Nassar, Ashraf ; Coppi, Francesca ; Maini, Arianna ; Grossule, Francesca ; Mattioli, Anna Vittoria ; Boriani, Giuseppe

Myotonic dystrophy type 1 (MD1) is the most common form of muscular dystrophy in adults. MD1 is caused by the expansion of CTG repeats in the DMPK gene and affects various organs beyond muscles. We present a case of a patient with MD1 exhibiting features of metabolic syndrome (MetS), including insulin resistance and dyslipidemia. The patient was treated with PCSK9 inhibitors, ezetimibe, and bempedoic acid because of intolerance. Metabolic syndrome is more prevalent in patients with muscle disorders like MD1, primarily caused by the sedentary lifestyle associated with muscle weakness. Although no specific studies on MetS frequency in MD1 exist, data on its components are available. This case highlights the management of MetS in MD1 with innovative therapies. Managing metabolic syndrome in MD1 patients requires personalized therapies. This case introduces a promising therapeutic approach for statin-intolerant patients.

15 Nov 2024·Medicine

The role of integrin-related genes in atherosclerosis complicated by abdominal aortic aneurysm

Article

Author: Jin, Lei ; Qiu, Zhihuang ; Ma, Likang ; Tang, Lele ; Chen, Liangwan ; Hong, Degao

Increasingly, the shared risk factors and pathological processes of atherosclerosis and abdominal aortic aneurysm (AAA) are being recognized. The aim of our study was to identify the hub genes involved in the pathogenesis of atherosclerosis and AAA. The analysis was based on 2 gene expression profiles for atherosclerosis (GSE28829) and AAA (GSE7084), downloaded from the Gene Expression Omnibus database. Common differential genes were identified and an enrichment analysis of differential genes was conducted, with construction of protein–protein interaction networks, and identification of common hub genes, and predicted transcription factors. The analysis identified 133 differentially expressed genes (116 upregulated and 17 downregulated), with the enrichment analysis identifying a potential important role of integrins and chemokines in the common immune and inflammatory responses of atherosclerosis and AAA. Regulation of the complement and coagulation cascades and regulation of the actin cytoskeleton were associated with both diseases, with 10 important hub genes identified: TYROBP, PTPRC, integrin subunit beta 2, ITGAM, PLEK, cathepsin S, lymphocyte antigen 86, ITGAX, CCL4, and FCER1G. Findings identified a common pathogenetic pathway between atherosclerosis and AAA, with integrin-related genes playing a significant role. The common pathways and hub genes identified provide new insights into the shared mechanisms of these 2 diseases and can contribute to identifying new therapeutic targets and predicting the therapeutic effect of biological agents.

01 Nov 2024·International Dental Journal

Identification of Potential Biomarkers and Therapeutic Targets for Periodontitis

Article

Author: Zhu, Hanfang ; Huang, Haonan ; Xiong, Junkai ; Mou, Yunjie ; Hou, Shuhan ; Yang, Bin ; Chen, Xinyu ; Huoshen, Wuda ; Sun, Chen ; Yi, Sha ; He, Yahan ; Li, Chunhui

BACKGROUNDPeriodontitis is a chronic and multifactorial inflammatory disease. However, existing medications often lack sufficient therapeutic effects. The aim is to identify potential biomarkers and efficient therapeutic targets using Mendelian randomisation (MR) and single-cell analysis.METHODSMR analysis was conducted based on the cis-expression quantitative trait loci (cis-eQTLs) extracted from the eQTLGen Consortium and genome-wide association study (GWAS) data of periodontitis sourced from the Gene Lifestyle Interactions in Dental Endpoints (GLIDE) consortium (17,353 cases, 28,210 controls). Subsequently, colocalisation analysis was employed to detect whether genes and periodontitis shared the same casual variant. Finally, enrichment analysis, protein-protein interaction (PPI) networks, drug prediction, phenome-wide association study (PheWAS), molecular docking, and single-cell analysis were conducted to validate the significance of target genes.RESULTSFourteen drug targets were significant related with periodontitis in MR analysis. Following the colocalisation and summary-data-based MR (SMR) analysis, 3 targets (S100A12, S100A9, and S100A8) were classified into tier 1 with strong evidence, 6 therapeutic targets (ADAM12, ADHFE1, BLK, HEBP1, SERPINE2, and TEK) were classified into tier 2 with moderate evidence, and 5 therapeutic targets (LY86, MMEL1, S100B, SPP1, and TRIB3) were classified into tier 3 with convincing evidence. PheWAS analysis showed that only TEK and SPP1 in tier 2 may induce side effects, including cardiometabolic and oncological issues. Molecular docking demonstrated strong binding between drugs and their respective protein targets. In the single-cell analysis, 5 target genes (HEBP1, LY86, S100A8, S100A9, and S100A12) exhibited enrichment in monocytes, while BLK and LY86 were primarily enriched in B cells.CONCLUSIONThe study identified 14 potential therapeutic targets for periodontitis. Among these, 3 therapeutic targets (S100A12, S100A9, and S100A8) demonstrated robust and well-supported results. Drugs designed to target these genes have a higher possibility of success in clinical trials, which are hopeful for prioritising periodontitis drug development.

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LY86

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