<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Design</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.2025050008</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>冠心病患者肠道菌的通路协同分析</title><url>https://artdesignp.com/journal/MRP/3/5/10.61369/MRP.2025050008</url><author>郑兴艺,王雨菲,张睿,王新钰,刘跃娟</author><pub-date pub-type="publication-year"><year>2025</year></pub-date><volume>3</volume><issue>5</issue><history><date date-type="pub"><published-time>2025-05-20</published-time></date></history><abstract>冠心病（CHD）的发生与肠道菌群紊乱密切相关，但其协同作用机制尚未完全阐明。本研究通过整合多组学数据，筛选冠心病患者肠道菌群特征性物种及代谢通路，探讨菌群间协同作用对宿主代谢的影响。利用TOPSIS算法筛选出30个与CHD显著相关的核心菌群，并通过IGM平台和KEGG通路分析揭示其参与的脂代谢、炎症反应等关键通路。UniProt功能注释进一步表明，目标菌群代谢物（如短链脂肪酸、氧化三甲胺）可能通过调控宿主免疫及内皮功能影响CHD进程。本研究为揭示肠道菌群协同机制提供了新的理论依据，并为CHD的精准干预策略奠定基础。</abstract><keywords>冠心病,肠道菌群,TOPSIS分析,KEGG通路,代谢标志物,协同分析</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1]Kazemian N, Mahmoudi M, Halperin F,et al. Gut microbiota and cardiovascular disease: opportunities and challenges. Microbiome. 2020 Mar14;8(1):36.[2]Katsimichas T, Theofilis P, Tsioufis K,et al. Gut Microbiota and Coronary Artery Disease: Current Therapeutic Perspectives. Metabolites. 2023 Feb9;13(2):256.[3]Wang Z, Zhao Y. Gut microbiota derived metabolites in cardiovascular health and disease. Protein Cell. 2018 May;9(5):416-431.[4]Andrade C. The &amp;lt;i&amp;gt;P&amp;lt;/i&amp;gt; Value and Statistical Significance:Misunderstandings, Explanations, Challenges, and Alternatives. Indian J Psychol Med. 2019 May-Jun;41(3):210-215. doi: 10.4103/IJPSYM.IJPSYM_193_19.[5]Jiang XC, Liu J. Sphingolipid metabolism and atherosclerosis. Handb ExpPharmacol. 2013;(216):133-46.[6]Won JS, Singh AK, Singh I. Lactosylceramide: a lipid second messenger inneuroinflammatory disease. J Neurochem. 2007 Nov;103 Suppl 1:180-91.[7]You X, Gao B. Association between Intestinal Flora Metabolites and Coronary Artery Vulnerable Plaque Characteristics in Coronary Heart Disease. Br J Hosp Med (Lond).2025 Mar 26;86(3):1-13.[8]Manzo OL, Nour J, Sasset L, et al. Rewiring Endothelial Sphingolipid Metabolism to Favor S1P Over Ceramide Protects From Coronary Atherosclerosis. Circ Res. 2024 Apr12;134(8):990-1005.[9]Choi RH, Tatum SM, Symons JD, Summers SA, Holland WL. Ceramides and other sphingolipids as drivers of cardiovascular disease. Nat Rev Cardiol. 2021 Oct;18(10):701-711.[10]Zhang R ,Ji X ,Tang Y , et al.Chitooligosaccharides Ameliorate Glomerular Mesangial Proliferation and Inflammation in IgA Nephropathy by Blocking S1PR1/S1PR3 Pathway[J/OL].Food Science and Human.[11] 廖晶, 周佳, 李龙.S1P在特发性肺纤维化中的研究进展[J].临床肺科杂志,2025,30(04):606-611.[12]Wang Z, Zhao Y. Gut microbiota derived metabolites in cardiovascular health and disease. Protein Cell. 2018 May;9(5):416-431. doi:10.1007/s13238-018-0549-0. Epub 2018 May 3.[13] 王琳. 稳定型冠心病患者肠道菌群变化特点的研究[D]. 西安医学院,2020.</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
