癌症中的炎性小体和自噬:解锁靶向治疗。

IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY
Jitendra Gupta, Mohammed Hashim Mohammed, Tawfeeq Alghazali, Subasini Uthirapathy, Roopashree R, Vishal Thakur, Manpreet Kaur, K Satyam Naidu, Aziz Kubaev, Mahmoud Mussleh Al-Mukhtar
{"title":"癌症中的炎性小体和自噬:解锁靶向治疗。","authors":"Jitendra Gupta, Mohammed Hashim Mohammed, Tawfeeq Alghazali, Subasini Uthirapathy, Roopashree R, Vishal Thakur, Manpreet Kaur, K Satyam Naidu, Aziz Kubaev, Mahmoud Mussleh Al-Mukhtar","doi":"10.1007/s00210-025-04184-x","DOIUrl":null,"url":null,"abstract":"<p><p>This study clarifies the interaction between autophagy and inflammasome within the cancer framework. The inflammasome generates pro-inflammatory cytokines to direct the immune response to pathogens and cellular stressors. Autophagy maintains cellular homeostasis and can either promote or inhibit cancer. These pathways interact to affect tumorigenesis, immune responses, and therapy. Autophagy controls inflammasome activity by affecting cancer pathogenesis and tumor microenvironment inflammation, highlighting novel cancer therapeutic approaches. Recent studies indicate that modulating autophagy and inflammasome pathways can boost anti-cancer immunity, reduce drug-resistance, and improve therapeutic efficacy. Recent studies indicate modulating inflammasome and autophagy pathways can augment anti-cancer immunity, mitigate therapy resistance, and improve treatment efficacy. Cancer research relies on understanding the inflammasome-autophagy relationship to develop targeted therapies that enhance anti-tumor efficacy and reduce inflammatory symptoms. Customized therapies may improve outcomes based on autophagy gene variations and inflammasome polymorphisms. This study investigates autophagy pathways and the inflammasome in tumor immunopathogenesis, cytokine function, and cancer therapeutic strategies, highlighting their significance in cancer biology and treatment.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"13295-13320"},"PeriodicalIF":3.1000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Inflammasomes and autophagy in cancer: unlocking targeted therapies.\",\"authors\":\"Jitendra Gupta, Mohammed Hashim Mohammed, Tawfeeq Alghazali, Subasini Uthirapathy, Roopashree R, Vishal Thakur, Manpreet Kaur, K Satyam Naidu, Aziz Kubaev, Mahmoud Mussleh Al-Mukhtar\",\"doi\":\"10.1007/s00210-025-04184-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>This study clarifies the interaction between autophagy and inflammasome within the cancer framework. The inflammasome generates pro-inflammatory cytokines to direct the immune response to pathogens and cellular stressors. Autophagy maintains cellular homeostasis and can either promote or inhibit cancer. These pathways interact to affect tumorigenesis, immune responses, and therapy. Autophagy controls inflammasome activity by affecting cancer pathogenesis and tumor microenvironment inflammation, highlighting novel cancer therapeutic approaches. Recent studies indicate that modulating autophagy and inflammasome pathways can boost anti-cancer immunity, reduce drug-resistance, and improve therapeutic efficacy. Recent studies indicate modulating inflammasome and autophagy pathways can augment anti-cancer immunity, mitigate therapy resistance, and improve treatment efficacy. Cancer research relies on understanding the inflammasome-autophagy relationship to develop targeted therapies that enhance anti-tumor efficacy and reduce inflammatory symptoms. Customized therapies may improve outcomes based on autophagy gene variations and inflammasome polymorphisms. This study investigates autophagy pathways and the inflammasome in tumor immunopathogenesis, cytokine function, and cancer therapeutic strategies, highlighting their significance in cancer biology and treatment.</p>\",\"PeriodicalId\":18876,\"journal\":{\"name\":\"Naunyn-Schmiedeberg's archives of pharmacology\",\"volume\":\" \",\"pages\":\"13295-13320\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2025-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Naunyn-Schmiedeberg's archives of pharmacology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s00210-025-04184-x\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/5/1 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"PHARMACOLOGY & PHARMACY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Naunyn-Schmiedeberg's archives of pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00210-025-04184-x","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/5/1 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0

摘要

本研究阐明了癌症框架内自噬与炎性体之间的相互作用。炎性小体产生促炎性细胞因子,指导免疫应答病原体和细胞应激源。自噬维持细胞内稳态,可以促进或抑制癌症。这些途径相互作用影响肿瘤发生、免疫反应和治疗。自噬通过影响癌症发病机制和肿瘤微环境炎症来控制炎性体活性,突出了新的癌症治疗方法。最近的研究表明,调节自噬和炎性体途径可以增强抗癌免疫,降低耐药,提高治疗效果。最近的研究表明,调节炎性体和自噬途径可以增强抗癌免疫,减轻治疗抵抗,提高治疗效果。癌症研究依赖于对炎性小体-自噬关系的理解,以开发靶向治疗,增强抗肿瘤疗效,减轻炎症症状。定制治疗可以改善基于自噬基因变异和炎性体多态性的结果。本研究探讨了自噬途径和炎性体在肿瘤免疫发病机制、细胞因子功能和肿瘤治疗策略中的作用,强调了它们在肿瘤生物学和治疗中的重要意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inflammasomes and autophagy in cancer: unlocking targeted therapies.

This study clarifies the interaction between autophagy and inflammasome within the cancer framework. The inflammasome generates pro-inflammatory cytokines to direct the immune response to pathogens and cellular stressors. Autophagy maintains cellular homeostasis and can either promote or inhibit cancer. These pathways interact to affect tumorigenesis, immune responses, and therapy. Autophagy controls inflammasome activity by affecting cancer pathogenesis and tumor microenvironment inflammation, highlighting novel cancer therapeutic approaches. Recent studies indicate that modulating autophagy and inflammasome pathways can boost anti-cancer immunity, reduce drug-resistance, and improve therapeutic efficacy. Recent studies indicate modulating inflammasome and autophagy pathways can augment anti-cancer immunity, mitigate therapy resistance, and improve treatment efficacy. Cancer research relies on understanding the inflammasome-autophagy relationship to develop targeted therapies that enhance anti-tumor efficacy and reduce inflammatory symptoms. Customized therapies may improve outcomes based on autophagy gene variations and inflammasome polymorphisms. This study investigates autophagy pathways and the inflammasome in tumor immunopathogenesis, cytokine function, and cancer therapeutic strategies, highlighting their significance in cancer biology and treatment.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
6.20
自引率
5.60%
发文量
142
审稿时长
4-8 weeks
期刊介绍: Naunyn-Schmiedeberg''s Archives of Pharmacology was founded in 1873 by B. Naunyn, O. Schmiedeberg and E. Klebs as Archiv für experimentelle Pathologie und Pharmakologie, is the offical journal of the German Society of Experimental and Clinical Pharmacology and Toxicology (Deutsche Gesellschaft für experimentelle und klinische Pharmakologie und Toxikologie, DGPT) and the Sphingolipid Club. The journal publishes invited reviews, original articles, short communications and meeting reports and appears monthly. Naunyn-Schmiedeberg''s Archives of Pharmacology welcomes manuscripts for consideration of publication that report new and significant information on drug action and toxicity of chemical compounds. Thus, its scope covers all fields of experimental and clinical pharmacology as well as toxicology and includes studies in the fields of neuropharmacology and cardiovascular pharmacology as well as those describing drug actions at the cellular, biochemical and molecular levels. Moreover, submission of clinical trials with healthy volunteers or patients is encouraged. Short communications provide a means for rapid publication of significant findings of current interest that represent a conceptual advance in the field.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信