Article(id=1276976090535039028, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20251013.501, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1747929600000, receivedDateStr=2025-05-23, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384425051, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384425051, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384425051, creator=13701087609, updateTime=1782384425051, updator=13701087609, issue=Issue{id=1276976057215488893, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='2', pageStart='301', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1768406400000', pubDateStr='2026-01-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782384417107, creator='13701087609', updateTime=1782384524478, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976507658563977, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976507658563978, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=413, endPage=420, ext={EN=ArticleExt(id=1276976090723782710, articleId=1276976090535039028, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Etiology, pathogenesis, and syndrome-based treatment of mitochondrial dysfunction in metabolic-associated fatty liver disease based on theory of "harmful hyperactivity and responding inhibition", columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

Mitochondrial dysfunction is a key pathological mechanism in metabolic-associated fatty liver disease (MAFLD), and regulating mitochondrial function to restore normal activity is an important therapeutic strategy. The theory of "harmful hyperactivity and responding inhibition" is a classical TCM principle that explains cyclical patterns in nature, interprets physiological and pathological phenomena in the human body, and guides TCM clinical diagnosis and treatment. The mechanism of mitochondrial dysfunction closely aligns with the process described in this theory as when the responding element fails to control, the hyperactive element becomes harmful. Based on the relationship between mitochondrial function and the TCM pathogenesis of MAFLD, and applying the "harmful hyperactivity and responding inhibition" framework, this study proposes that MAFLD originates from spleen deficiency impairing nutrient transport and failing to disperse essence, kidney Yang deficiency leading to impaired Qi transformation, and insufficient mutual regulation of the two, resulting in pathological products such as excessive accumulation of phlegm-turbidity, dampness, and blood stasis. These pathological changes manifest as mitochondrial dysfunction, including mtDNA damage, hepatocyte injury, lipid peroxidation, and mitochondrial accumulation. Clinically, MAFLD treatment follows the principle of regulating the responding element and restraining the hyperactive element: reinforcing the spleen earth to restore regulation, strengthening kidney water to nourish the kidneys and harmonize the liver, and addressing phlegm-stasis obstruction and hyperactivity through blood-activating and phlegm-resolving therapies. By modulating mitochondrial structure and function, this approach improves hepatic lipid metabolism, reduces oxidative stress, and alleviates inflammatory responses, achieving multi-target therapeutic effects. This study provides new theoretical foundations and practical strategies for integrated TCM-western medicine treatment of MAFLD.

, authors=null, authorsList=Kun-lan LIANG, Ling-ling LUO, Jing-jing HUANG, Hong-na HUANG, De-wen MAO, authorCompany=null, correspAuthors=Jing-jing HUANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1276976091373899833, articleId=1276976090535039028, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=基于“亢害承制”理论探讨代谢相关脂肪性肝病线粒体功能障碍的因机证治, columnId=1276975957151977760, journalTitle=中国中药杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

线粒体功能障碍是代谢相关脂肪性肝病（MAFLD）的关键病理机制，调节线粒体功能使其恢复正常运行是治疗该病的重要策略。“亢害承制”理论是阐释自然界周期性变化规律、解释人体生理病理现象，以及指导中医临床诊疗的中医经典理论。线粒体功能障碍的发生机制与“亢害承制”理论中承者失制，亢者为害的过程高度契合。该文基于线粒体功能与MAFLD的中医病机联系，结合“亢害承制”理论，认为MAFLD的病机为脾虚失运，难以散精，肾阳虚衰，气化无力，二者承制不足，反聚为痰浊、湿邪、瘀血亢为害的病理产物，表现为线粒体DNA损伤、肝细胞受损以及脂质过氧化物累积、线粒体堆积等线粒体功能障碍的表现。临床上MAFLD以承者制之，平其所亢为治疗原则，扶脾土之制、壮肾水以滋肾调肝，承而制之；痰瘀阻滞、亢而为害为病之标，当治以活血化瘀祛痰，平其所亢，可以通过调节线粒体结构及功能，改善肝脏脂质代谢、氧化应激、炎症反应等方面，从而实现对MAFLD的多靶点治疗效应。该文旨在为中西医结合治疗MAFLD提供新的理论依据和实践路径。

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