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<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">JCNR</journal-id><journal-title-group><journal-title>Journal of Clinical and Nursing Research</journal-title></journal-title-group><issn>2208-3685</issn><eissn>2208-3693</eissn><publisher><publisher-name>Bio-Byword Scientific Publishing Pty. Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.26689/jcnr.v9i7.11479</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>The Emerging Influence of Intestinal Microecological Dynamics on the Pathogenesis and Progression of Hepatic Chronic Pathologies: Current Scientific Perspectives</title><url>https://artdesignp.com/journal/JCNR/9/7/10.26689/jcnr.v9i7.11479</url><author>QinShaoyan</author><pub-date pub-type="publication-year"><year>2025</year></pub-date><volume>9</volume><issue>7</issue><history><date date-type="pub"><published-time>2025-08-04</published-time></date></history><abstract>The intestinal microbiome, often characterized as humanity’s “secondary genome,” possesses a genetic repertoire that dwarfs the coding capacity of the human genome by orders of magnitude. The essential architecture of this system is constituted by a vast phylogenetic tapestry of luminal microorganisms, whose dynamic symbiosis serves as a critical determinant of intestinal mucosal homeostasis and functional fidelity. The past decade has witnessed a paradigm shift in biomedical sciences, wherein technological breakthroughs in microbial single-cell genomics and spatial metatranscriptomics have unveiled the gut ecosystem’s pivotal role in host physiology. Emerging evidence from gut-liver interface research demonstrates how microbial-derived signals, facilitated by the portal circulatory nexus, mechanistically contribute to the initiation and perpetuation of chronic hepatopathies. 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