Article(id=1292130344812179509, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.08.022, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1769011200000, receivedDateStr=2026-01-22, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997480823, onlineDateStr=2026-08-06, pubDate=1777305600000, pubDateStr=2026-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997480823, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997480823, creator=13701087609, updateTime=1785997480823, updator=13701087609, issue=Issue{id=1292130221843571059, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='8', pageStart='1051', pageEnd='1200', issueExtLink='null', onlineDate='null', pubDate='1777305600000', pubDateStr='2026-04-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997451505, creator='13701087609', updateTime=1786014411018, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201355276480844, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201355276480845, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1189, endPage=1195, ext={EN=ArticleExt(id=1292130345021894710, articleId=1292130344812179509, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Mechanisms of autophagy in the pharmacological treatment of bladder cancer and research status of Chinese herbal medicine intervention, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=
Pharmacological treatment of bladder cancer (BC), including intravesical chemotherapy, systemic chemotherapy, chemoradiotherapy, and immunotherapy, still faces major challenges such as high recurrence rates, drug resistance, and treatment-related toxicities. As an important adaptive response under therapeutic stress, autophagy exerts a dual role in BC; it may cooperate with apoptosis and other pathways to mediate tumor cell death, or function as protective autophagy to promote cell survival and drive drug resistance. Therefore, strategies aimed at inducing lethal autophagy or inhibiting therapy-induced protective autophagy/autophagic flux blockade have emerged as potential approaches to optimize treatment response. Active components and compound formulas of traditional Chinese medicine can modulate autophagy through signaling pathways such as AMP-activated protein kinase/mechanistic target of rapamycin (AMPK/mTOR), and have shown potential to suppress tumor growth, enhance therapeutic sensitivity, and reduce toxicity. However, current evidence is still largely limited to in vitro and animal studies, criteria for autophagic flux evaluation remain inconsistent, and systematic studies on pharmacokinetics/pharmacodynamics (PK/PD), drug-drug interactions, and safety are lacking. Based on a systematic review of previous basic and preclinical studies, this article focuses on the representative molecular mechanisms by which active components and compound formulas of traditional Chinese medicine regulate autophagy, as well as their potential benefits and major limitations in the pharmacological treatment of BC, and further proposes possible directions for subsequent combination therapy and optimization of therapeutic strategies from the perspective of clinical pharmacology.
, authors=Gang-gang LU
1, Sheng-long LI
1, Peng-dong YIN
1, Guang-wei JIN
1, Huan WANG
1, Jiu-yun ZHOU
2a, Yong-qiang ZHAO
2a, Yun-peng JIA
2a, Xi-xiang LI
2b, authorsList=Gang-gang LU, Sheng-long LI, Peng-dong YIN, Guang-wei JIN, Huan WANG, Jiu-yun ZHOU, Yong-qiang ZHAO, Yun-peng JIA, Xi-xiang LI, authorCompany=null, correspAuthors=Jiu-yun ZHOU, Yong-qiang ZHAO, 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=1292130345286135863, articleId=1292130344812179509, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=细胞自噬在膀胱癌药物治疗中的作用机制及中药干预研究现状, columnId=1246531408819278046, journalTitle=中国临床药理学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=
目的 膀胱癌(BC)的药物治疗(含膀胱灌注化疗、化疗及放化疗/免疫治疗等)仍面临复发率高、耐药与毒副反应等问题。细胞自噬作为治疗应激下重要的适应性反应过程,在BC中呈“双相效应”:既可能与凋亡等通路协同介导细胞死亡,也可能形成保护性自噬促进存活并驱动耐药。因此,围绕“诱导致死性自噬”或“抑制治疗诱导的保护性自噬/阻断自噬流”的策略,成为优化药物治疗反应的潜在方向。中药活性成分与复方可通过腺苷酸活化蛋白激酶/哺乳动物雷帕霉素靶蛋白(AMPK/mTOR)等相关信号通路影响自噬过程,并在一定程度上表现出抑制肿瘤生长或增敏减毒的潜力。然而,现有研究证据多停留于体外/动物实验,自噬流评价标准不统一,且缺乏系统的药代动力学/药效学(PK/PD)、药物相互作用与安全性研究。本文在系统梳理既往基础与临床前研究的基础上,重点概述中药活性成分与复方调控细胞自噬的代表性分子机制及其在BC药物治疗中的潜在获益与主要局限,并尝试从临床药理学角度提出后续联合用药与方案优化的思路。
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1, 殷鹏东
1, 金广炜
1, 王欢
1, 周九云
2a, 赵永强
2a, 贾云鹏
2a, 李喜香
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卢刚刚(1997-),男,硕士研究生,主要从事泌尿外科疾病诊治与研究
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