Article(id=1291707249970405438, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707045514858818, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.23.013, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1753977600000, receivedDateStr=2025-08-01, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896607152, onlineDateStr=2026-08-05, pubDate=1765900800000, pubDateStr=2025-12-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896607152, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896607152, creator=13701087609, updateTime=1785896607152, updator=13701087609, issue=Issue{id=1291707045514858818, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='23', pageStart='3301', pageEnd='3450', issueExtLink='null', onlineDate='null', pubDate='1765900800000', pubDateStr='2025-12-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896558407, creator='13701087609', updateTime=1785896663780, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707487678390577, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707045514858818, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707487682584882, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707045514858818, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3391, endPage=3398, ext={EN=ArticleExt(id=1291707250792489023, articleId=1291707249970405438, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research status of salidroside reprogramming myocardial immune-inflammatory balance by targeting the T cell-macrophage interaction network, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Myocardial injury is frequently associated with an exacerbated cardiac-specific inflammatory response, leading to an imbalance in immune micro environment homeostasis. T cells and macrophages recruited to the site of injury constitute the primary components of inflammatory infiltration. Both the polarization status of macrophages and the differentiation levels of inflammatory T cells exhibit plasticity, transitioning from pro-inflammatory to anti-inflammatory phenotypes during the disease course. However, under conditions of intensified inflammation and immune dysregulation, a persistent pro-inflammatory state is maintained, characterized by M1 macrophages and helper T cell 1 (Th1)/Th17/Th22 cells, along with group 3 innate lymphoid cells (ILC3s). Salidroside (SAL) exerts antioxidant, anti-inflammatory, immunomodulatory, and anti-apoptotic effects on cardiomyocytes. This review aims to analyze the mechanism by which the single molecule SAL simultaneously reprograms the crosstalk balance between the three key cellular components (macrophages-T cells-cardiomyocytes) within the inflammatory microenvironment. Furthermore, it summarizes SAL’s mechanism of alleviating myocardial immune imbalance and associated inflammatory injury. This is achieved through blockade of the signal transducer and activator of transcription 3 (STAT3)/Th17/Interleukin-22 through type 2 cytokine receptor complex(IL-22-IL-22R) pro-inflammatory axis, promotion of macrophage polarization towards an anti-inflammatory phenotype, and modulation of T cell differentiation.

, authors=Yue ZHANG¹, Rui-fan YANG², Nan WANG³, authorsList=Yue ZHANG, Rui-fan YANG, Nan WANG, authorCompany=null, correspAuthors=Nan WANG, 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=1291707253728501824, articleId=1291707249970405438, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=红景天苷靶向T细胞-巨噬细胞互作网络调控心肌免疫炎症的研究现状, columnId=1246531408819278046, journalTitle=中国临床药理学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

心脏特征性的炎症反应加剧造成的微环境免疫稳态失衡常导致心肌损伤，趋化至损伤区的T细胞及巨噬细胞是炎症浸润的主要成分。巨噬细胞的极化及炎症T细胞激活与分化存在可塑性，可随病程完成由促炎到抗炎的改变；但当炎症加剧免疫失衡时将保持M1型巨噬细胞和辅助性T细胞（Th1/17/22）、3型固有淋巴样细胞（ILC3）等促炎状态。红景天苷（SAL）具有抗氧化、抗炎、免疫调节及抑制心肌细胞凋亡作用。本文旨在阐明单一分子SAL重塑炎症微环境中三大细胞组分，维持巨噬细胞- T细胞-心肌细胞互作平衡的机制；总结SAL通过阻断信号转导及转录激活因子3（STAT3）/Th17/白介素-22及其受体（IL-22-IL-22R）炎症通路，有效促进巨噬细胞向抗炎表型极化并调节T细胞分化，以缓解心肌免疫失衡及其炎症相关损伤。

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张玥（2001-），女，硕士研究生，主要从事免疫学方向单细胞测序相关的研究

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张玥（2001-），女，硕士研究生，主要从事免疫学方向单细胞测序相关的研究

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