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Article(id=1203033497289056754, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2023.05.0602, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1645027200000, receivedDateStr=2022-02-17, revisedDate=null, revisedDateStr=null, acceptedDate=1657209600000, acceptedDateStr=2022-07-08, onlineDate=1764755137035, onlineDateStr=2025-12-03, pubDate=1685203200000, pubDateStr=2023-05-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1764755137035, onlineIssueDateStr=2025-12-03, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1764755137035, creator=13701087609, updateTime=1764755137035, updator=13701087609, issue=Issue{id=1203033494428541350, tenantId=1146029695717560320, journalId=1189873630562394117, year='2023', volume='48', issue='5', pageStart='489', pageEnd='626', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1764755136353, creator=13701087609, updateTime=1764756085669, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1203037476202967229, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1203037476202967230, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=602, endPage=608, ext={EN=ArticleExt(id=1203033497591046659, articleId=1203033497289056754, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Hazard and mediation mechanism of exosomes in the cachexia inflammatory response, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Cachexia is a serious chronic wasting syndrome, which is a common complication of cancer, end-stage heart failure and other diseases. The abnormal inflammatory response in the process of cachexia plays an important role in the loss of muscle and fat, the proliferation and metastasis of tumors. In recent years, it has been found that microRNA and long non-coding RNA (lncRNA) carried in exosomes can mediate cell-to-cell communication, activate related signaling pathway to secrete various inflammatory factors. It mediates the inflammatory response of cachexia, affects the formation of local and distal inflammatory microenvironment, promotes tumor cell proliferation, metastasis and inhibits its apoptosis, thereby accelerating the progression of cachexia. This review mainly summarizes the relationship between exosome and cachexia inflammation response, the harm of cachexia inflammation response and the mechanism of action, and provides new ideas for preventing it and slowing down the cachexia progress.

, correspAuthors=Du-Fang Ma, authorNote=null, correspAuthorsNote=
* E-mail:
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恶病质是一种严重的慢性消耗性状态，是恶性肿瘤、终末期心力衰竭等疾病常见的并发症。恶病质进程中异常的炎症反应在肌肉、脂肪丢失及肿瘤增殖转移中发挥重要作用。近年研究发现，外泌体内携带的微小核糖核酸（microRNA）、长链非编码核糖核酸（lncRNA）等成分可通过介导细胞间通信，激活相关信号通路，促进多种炎性因子的分泌，从而介导恶病质炎症反应，影响局部和远端炎性微环境的形成，促进肿瘤细胞增殖、转移并抑制其凋亡，加速恶病质的进展。本文对外泌体与恶病质炎症反应的关系、恶病质炎症反应的危害及外泌体通过调控Toll样受体、核因子κB（NF-KB）、CC趋化因子配体2（CCL2）等分子和通路诱发恶病质炎症反应的作用机制进行综述，旨在为预防恶病质炎症反应及减缓恶病质进展提供新的思路。

, correspAuthors=马度芳, authorNote=null, correspAuthorsNote=
马度芳，E-mail:
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吴涛，硕士研究生，主要从事心血管病理生理方面的研究

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吴涛，硕士研究生，主要从事心血管病理生理方面的研究

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吴涛，硕士研究生，主要从事心血管病理生理方面的研究

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miRNA. 微小核糖核酸；lncRNA. 长链非编码核糖核酸；PD-L1. 细胞程序性死亡蛋白-配体1；STAT3. 信号转导及转录激活蛋白3；SOCS. 细胞因子信号抑制物；TNF-α. 肿瘤坏死因子-α；IL-6. 白细胞介素-6；NF-κB. 核因子κB；肿瘤细胞来源的外泌体携带的miRNA、lncRNA等成分可通过靶向受体细胞的跨膜蛋白Toll样受体、PD-L1，激活细胞质内转录因子STAT3、NF-κB而介导细胞炎性因子的产生，并刺激细胞因子SOCS负反馈调节STAT信号通路，使免疫细胞异常活化，表达和分泌多种促炎细胞因子(如TNF-α、IL-6等)，最终导致恶病质炎症反应的发生

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外泌体在恶病质炎症反应中的作用及机制研究进展
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吴涛 1 , 徐圣洁 1 , 李晓 2 , 王咏 2 , 马度芳 2, *
解放军医学杂志 | 综述 2023,48(5): 602-608
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解放军医学杂志 | 综述 2023, 48(5): 602-608
外泌体在恶病质炎症反应中的作用及机制研究进展
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吴涛1, 徐圣洁1, 李晓2, 王咏2, 马度芳2, *
作者信息
  • 1山东中医药大学第一临床医学院，山东济南 250000
  • 2山东中医药大学附属医院心血管病科，山东济南 250014

    • 吴涛，硕士研究生，主要从事心血管病理生理方面的研究

通讯作者:

马度芳，E-mail:
Hazard and mediation mechanism of exosomes in the cachexia inflammatory response
Tao Wu1, Sheng-Jie Xu1, Xiao Li2, Yong Wang2, Du-Fang Ma2, *
Affiliations
  • 1The First Clinical College, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250000, China
  • 2Department of Cardiovascular Disease, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250014, China
出版时间: 2023-05-28 doi: 10.11855/j.issn.0577-7402.2023.05.0602
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摘要
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恶病质是一种严重的慢性消耗性状态，是恶性肿瘤、终末期心力衰竭等疾病常见的并发症。恶病质进程中异常的炎症反应在肌肉、脂肪丢失及肿瘤增殖转移中发挥重要作用。近年研究发现，外泌体内携带的微小核糖核酸（microRNA）、长链非编码核糖核酸（lncRNA）等成分可通过介导细胞间通信，激活相关信号通路，促进多种炎性因子的分泌，从而介导恶病质炎症反应，影响局部和远端炎性微环境的形成，促进肿瘤细胞增殖、转移并抑制其凋亡，加速恶病质的进展。本文对外泌体与恶病质炎症反应的关系、恶病质炎症反应的危害及外泌体通过调控Toll样受体、核因子κB（NF-KB）、CC趋化因子配体2（CCL2）等分子和通路诱发恶病质炎症反应的作用机制进行综述，旨在为预防恶病质炎症反应及减缓恶病质进展提供新的思路。

恶病质炎症反应  /  外泌体  /  肿瘤微环境  /  炎性因子

Cachexia is a serious chronic wasting syndrome, which is a common complication of cancer, end-stage heart failure and other diseases. The abnormal inflammatory response in the process of cachexia plays an important role in the loss of muscle and fat, the proliferation and metastasis of tumors. In recent years, it has been found that microRNA and long non-coding RNA (lncRNA) carried in exosomes can mediate cell-to-cell communication, activate related signaling pathway to secrete various inflammatory factors. It mediates the inflammatory response of cachexia, affects the formation of local and distal inflammatory microenvironment, promotes tumor cell proliferation, metastasis and inhibits its apoptosis, thereby accelerating the progression of cachexia. This review mainly summarizes the relationship between exosome and cachexia inflammation response, the harm of cachexia inflammation response and the mechanism of action, and provides new ideas for preventing it and slowing down the cachexia progress.

cachexia inflammation response  /  exosome  /  tumor microenvironment  /  inflammatory factor
吴涛, 徐圣洁, 李晓, 王咏, 马度芳. 外泌体在恶病质炎症反应中的作用及机制研究进展. 解放军医学杂志, 2023 , 48 (5) : 602 -608 . DOI: 10.11855/j.issn.0577-7402.2023.05.0602
Tao Wu, Sheng-Jie Xu, Xiao Li, Yong Wang, Du-Fang Ma. Hazard and mediation mechanism of exosomes in the cachexia inflammatory response[J]. Medical Journal of Chinese People’s Liberation Army, 2023 , 48 (5) : 602 -608 . DOI: 10.11855/j.issn.0577-7402.2023.05.0602
正文
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恶病质是一种以骨骼肌萎缩、脂肪丢失及厌食症为主要特点，伴有代谢紊乱及全身系统性炎症的临床综合征[1]。恶病质通常与一些潜在的慢性退行性疾病有关，如癌症、慢性阻塞性肺疾病、慢性肾衰竭和终末期心力衰竭等。恶病质病程的发展往往难以被营养支持疗法所逆转，且会逐渐破坏人体生理功能，造成全身多脏器的进行性衰竭。同时，恶病质炎性微环境是肿瘤增殖、侵袭和转移的良好土壤[2]，是加速恶病质发展的重要条件。恶病质炎症反应不仅可在肿瘤微环境中维持肿瘤细胞的增殖率、刺激血管生成并抑制细胞凋亡，而且可影响细胞间信息传递和基因表达，间接导致肌肉萎缩，以及肝脏和脂肪细胞行为的改变[3]。
越来越多的临床报告显示炎症标志物水平升高是不同疾病恶病质患者的共同特征[4]，与非恶病质患者比较，恶病质患者血清中超敏C反应蛋白(hypersensitive C-reactive protein，hs-CRP)、白细胞介素-6 (interleukin-6，IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α，TNF-α)和γ干扰素(interferon-γ，IFN-γ)等炎性因子表达水平升高[5-6]。因此，寻找恶病质炎症反应的相关治疗靶点可能有助于减缓恶病质进程，提高患者生存率。近年来外泌体与炎症反应的相关性得到了进一步验证，外泌体可直接作用于免疫细胞或通过触发免疫细胞膜上的受体，激活相关信号分子并介导炎性因子的产生，进而诱发炎症反应[7]。此外，在治疗方面通过在肿瘤微环境中调控外泌体介导炎症的相应分子机制以减缓恶病质进展，也已被报告为一种可行的策略[8]。本综述总结外泌体与恶病质炎症反应的相关性及其介导恶病质炎症反应的主要靶点与机制，旨在为预防和治疗恶病质炎症反应提供新的思路。
1 外泌体及其与恶病质炎症反应的相关性
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1.1 成分及功能
外泌体是直径40～150 nm的囊性载体，是多种疾病的新介质[9]，几乎存在于所有允许其运输的生物液体中，如血浆、唾液、尿液等。近年来，外泌体因其在细胞间传递生物成分的能力而受到越来越多的关注。与传统的细胞间通信方式不同，外泌体代表了基于分子货物的另一种通用的细胞间通信方式[10]。
外泌体可以运输多种分子，包括脂质、蛋白质和核酸，运载的分子被包裹在外泌体的脂质双层结构中，以保护它们免受环境中酶的降解，并促进其在细胞间的摄取[11]。其中微小核糖核酸(microRNA，miRNA)、信使核糖核酸(messenger RNA，mRNA)、长链非编码核糖核酸(long non-coding RNA，lncRNA)是介导恶病质炎症反应的关键因子。虽然外泌体最初被认为仅与废物处理有关[12]，然而，外泌体一旦释放到细胞外就可在不同的体液间进行循环，通过介导自分泌和旁分泌细胞间的串扰来实现通信效应，促使局部和远端微环境的改变，并通过调节受体细胞表型介导多种生理或病理过程[13-14]。恶病质时期肿瘤细胞来源的外泌体是改变肿瘤微环境和调节恶病质进展的重要因素，当正常细胞接触肿瘤来源的外泌体时，后者可通过重塑细胞外基质及刺激多种膜受体的信号转导影响受体细胞的表型[15]。有研究报告了外泌体诱导恶病质脂肪和肌肉组织异常消耗的作用机制[16-17]，但其在恶病质炎症反应中的作用仍有待进一步探索。
1.2 与恶病质炎症反应的相关性
越来越多的研究显示，外泌体与恶病质炎症反应的发生有着密不可分的关系。癌源性外泌体可改变肿瘤微环境，形成肿瘤原生态位，刺激环境中浸润性免疫细胞、基质细胞和内皮细胞的相互沟通，形成炎症微环境，从而促进肿瘤生长、转移及血管生成，加速恶病质进程。体外研究显示，血清中外泌体的表达量与肿瘤恶病质的进展呈正相关。Panigrahi等[18]通过纳米粒子示踪仪分析前列腺癌恶病质患者的血清，结果显示其外泌体浓度比健康人增高了3.2倍(P<0.05)，进一步研究发现血清中前列腺癌细胞分泌的外泌体可强烈诱导巨噬细胞的致炎M2表型，并且体外钙成像也显示被外泌体诱导的神经元胞质中Ca2+明显增加进而导致神经炎性反应。另有研究对56例宫颈癌恶病质患者进行血浆外泌体RNA测序，结果显示，外泌体内miRNAs和mRNAs的表达量与宫颈癌炎症反应的诱发及癌症转移微环境的塑造密切相关，并进一步检测出外泌体运载的miR1228-5p、miR-146a-3p和miR-6815-5p等成分参与了激活宫颈癌恶病质炎症反应和免疫抑制状态[19]，提示外泌体可通过其运载的miRNA等成分经血液运输来调控恶病质炎症反应的发生。体内研究则显示，胃癌细胞来源的外泌体在胃癌恶病质患者肝脏中可参与中性粒细胞的募集，并活化巨噬细胞中核因子κB(nuclear factor kappa-B，NF-κB)，使促炎因子如IL-6和TNF-α的表达增加，诱导肿瘤炎症微环境，促进胃癌细胞向肝脏的转移及加速恶病质进程[20-22]。由此可见，外泌体可通过某些机制参与免疫细胞的募集活化及炎性因子的分泌而诱发炎症，塑造炎性微环境，促进肿瘤增殖转移，进一步加速恶病质进程。
2 在恶病质炎症反应中的危害
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外泌体诱发的全身炎症反应与恶病质不同阶段异常的体重下降、肿瘤增殖转移及较差的预后密切相关[23]。癌症恶病质模型全身炎症与肌肉组织异常丢失的相关性已被广泛报道。在动物实验中，Walker256荷瘤恶病质大鼠与非荷瘤对照组比较，血浆中TNF-α和IL-6升高并表现出全身炎症反应，同时恶病质组后肢肌肉中与肌肉萎缩相关的肌萎缩素1(muscle atrophy F-box protein 1，Atrogin-1)和肌环指蛋白1(muscle-specific RINGfinger protein 1，MuRF-1)的基因和蛋白表达水平也相应增高[24]。同样，在原位膀胱癌小鼠模型中也观察到类似结果，在该模型动物的肌肉组织中检测到炎性细胞因子TNF-α、IL-6和IL-1β水平增高，以及包括NF-κB在内的促炎途径的激活，而这些观察结果与叉头蛋白O3(forkhead box O3，FOXO3)磷酸化水平下调平行，提示恶病质炎症反应环境中某些炎性因子可激活有关肌肉萎缩与代谢的信号，引发肌肉组织的异常代谢，使恶病质患者的肌肉组织进一步流失，加速恶病质进展[25]。在人体研究中，Abbass等[26]采用计算机断层扫描(computed tomography，CT)和双能X线吸收法(dual energy X-ray absorptiometry，DEXA)检测不同类型癌症的恶病质患者，结果显示，恶病质患者全身炎性因子增多与低骨骼肌指数具有明显的相关性，进一步验证了癌症恶病质患者异常的炎症反应与骨骼肌丢失之间的联系。
恶病质炎症反应不仅与恶病质肌肉萎缩联系密切，还参与引发恶病质进程中异常的脂肪代谢并增加机体的能量消耗。Abdullahi等[27]报告在恶病质小鼠腹股沟白色脂肪中脂肪棕色化基因解耦联蛋白1(uncoupling protein-1，UCP-1)、PR/SET结构域16(PRD1-BF-1-RIZ1 homologous domain-containing protein-16，PDRM16)等表达升高，进一步检测显示白色脂肪组织局部微环境中特定功能表型的M2巨噬细胞上调，提示恶病质炎症反应环境会刺激白色脂肪向棕色化表型的转化，促进机体产热，造成能量耗散；相反，在抑制白色脂肪组织局部微环境中的炎性因子后，脂肪组织棕色化基因的表达显著降低，提示抑制白色脂肪组织微环境中的炎症反应会减缓其棕色化进程，减少无意义的热量耗散。
恶病质时期肿瘤的异常增殖、转移也与炎症反应密切相关。外泌体可介导肿瘤细胞与微环境中远端细胞间的通信，通过循环将脂质、蛋白质、核酸和特定的信号分子转移到远端细胞，从而介导微环境中的炎症反应。肿瘤细胞外泌体可包装促炎和趋化介质，产生趋化性类固醇，调节免疫细胞不同表型的转化，诱导体内淋巴细胞激活和白细胞迁移，对转移前微环境进行重塑，从而增强癌细胞的增殖、转移能力[28]。体外研究显示，黑色素瘤细胞分泌的外泌体可被巨噬细胞吞噬，诱导巨噬细胞向M2表型转化，激活STAT3信号通路，刺激IL-10释放和PDL1上调而介导肿瘤炎性微环境，促进黑色素瘤转移及恶病质进展[29]。同样，体内研究也发现，胰腺癌恶病质患者衍生的外泌体可介导形成肝转移前炎症生态位而在肿瘤转移中发挥作用；外泌体可通过调节TNF-α和IL-12等炎性因子的表达，介导自身炎症反应，抑制免疫系统的抗肿瘤活性，从而促进肿瘤细胞的异常增殖和转移[30]。因此，外泌体介导的炎症反应在恶病质进展中的作用不容忽视，通过抑制外泌体对炎症反应的诱发，调控肿瘤转移前炎症微环境的形成，可能对缓解恶病质进程有重要意义。
3 对恶病质炎症反应的介导机制
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恶病质炎症反应的相关研究显示，外泌体包含的miRNA、lncRNA等可通过靶向受体蛋白，激活相关信号通路等机制来介导恶病质炎症反应，进而调控肿瘤转移前炎症微环境，促进肿瘤增殖、转移，加速恶病质进程(图1)。
3.1 Toll样受体(Toll-like receptors，TLR)
TLR多表达在巨噬细胞、树突状细胞等细胞表面，其介导的信号转导可导致免疫细胞异常活化，进而表达、分泌多种炎性因子如TNF-α、IL-6等。Fabbri等[31]的研究显示，miRNA除通过外泌体在细胞间转移，并与靶mRNA结合来调节受体细胞的炎性因子表达外，还可作为配体与肿瘤相关巨噬细胞(tumour-associated macrophages，TAM)表面的TLR结合，触发TLR介导的转移性炎症反应，形成恶病质炎症反应微环境，最终导致肿瘤的生长和转移，加速恶病质进程。Chow等[32]在携带异种移植人乳腺癌的小鼠中观察到，乳腺癌来源的外泌体可被腋窝淋巴结中的巨噬细胞内化，触发IL-6等炎性因子的表达，而在消融巨噬细胞的TLR受体后，小鼠腋窝淋巴结处微环境中的炎性因子表达与分泌减少，外泌体的促炎作用明显下降，提示TLR受体可能作为外泌体的靶点参与恶病质炎症反应。Casadei等[33]对脂肪肉瘤(liposarcoma，LPS)恶病质患者血浆样本的纳米串图谱分析显示，血浆IL-6水平升高与LPS来源的外泌体中miR-25-3p和miR-92a-3p表达上调有关；进一步研究发现其外泌体的促炎机制与TLR受体密切相关，用其外泌体来源的miR-25-3p和miR-92a-3p混合物处理正常和分离TLR7/8受体的小鼠腹腔巨噬细胞后，正常未分离组外泌体混合物可特异性促进巨噬细胞分泌IL-6，而分离TLR7/8受体的巨噬细胞中IL-6形成受到抑制。该结果提示恶病质患者外泌体中的某些miRNA可通过与巨噬细胞TLR受体结合，促使细胞分泌IL-6等炎性因子，参与恶病质炎症反应。上述研究表明，外泌体可通过TLR依赖的方式刺激TAM分泌炎性因子IL-6，诱导炎症微环境的形成，加速恶病质进展。
3.2 信号传导及转录激活蛋白3(signal transducer and activator of transcription3，STAT3)
STAT3是一种细胞质转录因子，其异常激活(如磷酸化)可诱发与慢性炎症有关的细胞因子、趋化因子和其他介质的表达与释放，如IL-6、巨噬细胞集落刺激因子(macrophage-stimulating factor，M-CSF)、前列腺素(prostaglandin，PG)和环氧合酶2(cyclooxygenase2，COX2)等。He等[34]的细胞实验结果显示，内质网在肝癌恶病质应激状态下释放的外泌体体外作用小鼠巨噬细胞系RAW264.7细胞24 h后，细胞内磷酸化STAT3蛋白的表达水平显著升高，采用STAT3抑制剂S3I-201阻断STAT3后，细胞中单核细胞趋化蛋白1(monocyte chemoattractant protein，MCP-1)、IL-6和IL-10等炎性因子的表达水平显著降低，提示STAT3激活可能是肝癌恶病质状态下内质网分泌外泌体介导炎症反应的一个潜在机制。在动物实验中，Chen等[35]进一步报告异种移植人卵巢癌模型鼠在注射含卵巢癌外泌体来源的miR-21-3p、miR-125b-5p和miR-181D-5p后，其肿瘤生长速度和累计死亡率均高于注射同体积磷酸盐缓冲液(PBS)的对照组，Western blotting检测结果显示注射外泌体组癌症小鼠的STAT3表达水平明显高于对照组，同时巨噬细胞M2极化程度和血清中IL-10等炎性因子表达量也较对照组升高，提示卵巢癌来源外泌体中的miR-21-3p、miR-125b-5p和miR-181D-5p可通过调控STAT3影响巨噬细胞M2极化和炎性因子的分泌而介导与维持促癌炎症环境，加速恶病质进程。
3.3 NF-κB
NF-κB是一种能调节多种炎症和免疫基因表达的诱导性转录调节因子，可与多种细胞因子基因的启动子特异性结合，调控其转录和表达，从而影响细胞周期、炎症反应和免疫应答等病理生理过程。Ghodrati等[36]对入胃癌组织标本进行RT-qPCR检测显示，组织中外泌体来源的lncRNA淋巴细胞白血病缺失基因1(lncRNA deleted in lymphocytic leukemia 1，lncRNA DLEU1)相对表达水平高于健康人群，并与NF-κB的表达水平显著相关，其相关系数随着癌症分期和恶病质程度的增加而提高。为了进一步确定外泌体介导的恶病质炎症反应与NF-κB激活的关系，Wu等[37]采用胃癌细胞来源的外泌体体外培养人髓系白血病单核细胞系THP-1细胞，结果显示肿瘤外泌体可显著上调巨噬细胞中NF-κB的磷酸化，ELISA检测显示经肿瘤外泌体处理的THP-1细胞中IL-6和TNF-α蛋白表达显著升高，而用NF-κB抑制剂BA117082阻断THP-1细胞NF-κB的磷酸化进程后，IL-6和TNF-α等炎性因子的表达受到显著抑制，提示NF-κB是联系恶病质炎症反应与肿瘤外泌体的关键信号分子之一，外泌体可通过激活NF-κB引起细胞炎性因子的表达介导炎症，进而促进恶病质炎症反应微环境的建立和肿瘤的迁移与侵袭。
3.4 细胞因子信号抑制物(suppressor of cytokine signaling，SOCS)
SOCS是一类由细胞产生、可反馈性阻断细胞因子信号转导过程的负性调节因子。SOCS可通过负调节多种细胞因子的信号转导，对体内多种免疫炎症反应的激活发挥调控作用。Song等[38]报告miR-9-5p在肾癌细胞来源的外泌体中广泛表达，并与肾癌炎症微环境及肾癌细胞的增殖和侵袭密切相关；进一步研究显示，肾癌细胞外泌体中miR-9-5p过表达可通过靶向和去调控SOCS4，减弱对Janus激酶/信号转换器和转录激活因子(Janus kinase/signal transducer and activator of transcription，JAK/STAT)通路的抑制作用，促进STAT3和JAK的磷酸化而介导炎症反应的发生，当加入miR-9-5p抑制剂时这种促炎作用被逆转，提示外泌体中miR-9-5p可能通过作用于SOCS4减弱对JAK/STAT通路的抑制以促进肾癌细胞的增殖和侵袭，加速恶病质进展。此外，还有研究显示肿瘤外泌体除通过影响SOCS表达导致JAK/STAT通路上调外，还可通过影响SOCS表达间接激活NF-κB 信号通路来参与恶病质炎症反应。Masoumi-Dehghi等[39]报告来自卵巢癌上皮细胞的含miRNA-141-3p 的外泌体可显著降低SOCS5的表达水平，在细胞实验中用人脐静脉内皮细胞(human umbilical vein endothelial cells，HUVEC)分别经过卵巢癌上皮细胞外泌体和PBS对照条件孵化48 h后，与PBS对照组比较，外泌体组HUVEC内NF-κB p65蛋白表达水平升高、SOCS5表达水平降低，提示卵巢癌上皮细胞含miRNA-141-3p的外泌体可能通过作用于SOCS5而调控NF-κB信号通路，介导内皮细胞炎性因子的分泌，创造卵巢癌细胞的炎症微环境，加速血管生成和卵巢癌进展。
3.5 细胞程序性死亡蛋白-配体1(programmed cell death 1 ligand 1，PD-L1)
PD-L1是大小为40 kD的第一型跨膜蛋白，可通过调控T细胞活性和细胞因子的产生参与肿瘤炎症微环境的形成，诱导肿瘤浸润和转移。在体外研究中，Cheng等[40]报告肝癌细胞来源的外泌体可上调THP-1分化的巨噬细胞中 PD-L1表达；流式细胞术检测显示外泌体组PD-L1表达量大约是PBS对照组的4倍，同时发现与肝癌细胞来源外泌体共培养的THP-1分化的巨噬细胞中IL-6、IL-10和TNF-α等炎性因子水平也较PBS对照组明显增高；进一步的体内研究显示，通过尾静脉向小鼠注射同剂量PBS或肝癌细胞来源的外泌体后，外泌体组小鼠腹腔巨噬细胞中PD-L1表达上调，而PBS组变化不明显，此外，外泌体组炎性因子如IL-6、TNF-α和IL-10的表达水平均高于PBS组。上述结果提示肝癌细胞来源的外泌体可能通过上调巨噬细胞中PD-L1的表达来介导肿瘤微环境的炎症反应，从而调控肝癌细胞的增殖与转移，加速恶病质进展。同样，Haderk等[41]在慢性淋巴细胞白血病(chronic lymphocytic leukemia，CLL)患者的血液中发现，单核细胞和巨噬细胞倾向于促肿瘤表型的程度与CLL来源外泌体的摄取有关，进一步的小鼠体内研究显示，CLL来源的外泌体在小鼠次级淋巴组织微环境中起中心作用，可通过上调PD-L1和炎性细胞因子促进单核细胞和巨噬细胞向促肿瘤表型转变，而在阻断PD-L1的结合位点后，小鼠微环境中炎性因子的上调得到控制，可减缓小鼠CLL的进展和恶病质进程，提示PD-L1可能成为外泌体介导恶病质炎症反应有效的治疗靶点。
3.6 CC趋化因子配体2(CC chemokine ligand 2，CCL2)
CCL2是CXC趋化因子家族中的小分子量细胞因子，可通过作用于CC趋化因子受体2(CC chemokine ligand receptor 2，CCR2)调控免疫细胞向肿瘤的迁移[42]，诱导炎症微环境，从而加速癌细胞的播散和扩张。Rogic等[43]采用乳腺癌恶病质炎症反应小鼠模型的研究显示，外泌体可介导CCL2在髓系细胞中高表达，进一步研究发现，其分泌水平与局部和系统内不同炎症细胞亚群的动员及微环境中外泌体的含量有关，尤其在转移部位单核细胞和巨噬细胞的募集以及转移前炎症微环境的形成中可发挥重要作用，相反，敲除CCL2基因可显著抑制恶病质小鼠模型的肿瘤生长和炎症表型，提示外泌体可能通过作用于CCL2来介导不同炎症细胞群的迁移，促进乳腺癌恶病质炎症反应微环境的建立。为进一步验证CCL2在外泌体诱发恶病质炎症反应微环境中的作用，Gu等[44]利用乳腺癌细胞外泌体来源的mir-200b-3p刺激乳腺癌荷瘤小鼠肺组织，结果显示外泌体中的miR-200b-3p可直接靶向肺组织细胞mRNA 3'末端非翻译区而抑制磷酸酶和肿瘤抑制因子，导致CCL2趋化因子的分泌升高，刺激单核细胞和巨噬细胞的募集及IL-6、PD-L1等炎性因子的表达，从而促进转移前炎性生态位的建立和乳腺癌细胞向肺组织的扩散；与正常乳腺癌荷瘤小鼠比较，在CCL2基因敲除的荷瘤小鼠中进行上述实验，结果显示其肺组织中招募的骨髓来源的抑制性细胞比例及炎性因子表达明显降低，肺转移明显减少，进一步提示外泌体中miR-200b-3p可通过靶向CCL2介导单核细胞和巨噬细胞的募集，提高炎性因子的表达水平，构建恶病质炎症反应微环境，促进乳腺癌细胞的肺组织转移，加速恶病质进展。
除了上述几种外泌体导致恶病质炎症反应的主要机制外，还有其他机制的相关报道。Li等[45]报告内毒素预处理的恶病质骨髓间充质干细胞来源的外泌体可刺激巨噬细胞向M1样表型的极化，并诱导T细胞向Th17细胞的促炎分化，同时微环境中凝血酶敏感蛋白1(thrombospondin-1，TSP-1)表达水平升高，而在抑制TSP-1的表达后，上述外泌体引起的促炎反应水平明显降低，提示TSP-1是影响癌症恶病质外泌体促炎调节能力的重要分子，外泌体可通过影响TSP-1表达介导炎症反应，从而改变肿瘤炎症微环境。此外，Li[46]报告胃癌恶病质患者来源的外泌体可在体外促进肿瘤细胞增殖和微环境炎症反应，Western blotting检测显示丝裂原活化蛋白激酶(mitogen-activated protein kinase，MAPK)的表达随外泌体浓度升高和胃癌细胞增殖而显著上调，提示外泌体可能通过激活MAPK信号通路介导炎性因子的生成，促进胃癌细胞的增殖和侵袭，加速恶病质进展。
4 总结与展望
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综上所述，外泌体在介导恶病质炎症反应中的作用不容忽视，恶病质时全身异常的炎症反应与外泌体的诱导密切相关。恶病质炎症反应会促进肌肉和脂肪的异常丢失，造成高消耗的虚弱状态，同时恶病质时肿瘤的炎症微环境会加速肿瘤增殖与侵袭，促进肿瘤转移，推动恶病质进程。在恶病质时期，外泌体可通过调控TLR、STAT3、NF-κB、CCL2等分子和通路介导肿瘤微环境中炎性因子的形成，是引起恶病质异常炎症微环境的重要原因。因此，在恶病质炎症反应的临床预防与治疗中，明确外泌体介导恶病质炎症反应的机制，有助于开发相应的阻断药物减缓肿瘤炎症微环境形成，进而抑制肿瘤的恶性增殖甚至阻断恶病质进程。
基金
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  • 国家自然科学基金(82004280)
  • 国家自然科学基金(82074388)
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2023年第48卷第5期
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doi: 10.11855/j.issn.0577-7402.2023.05.0602
  • 接收时间：2022-02-17
  • 首发时间：2025-12-03
  • 出版时间：2023-05-28
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  • 收稿日期：2022-02-17
  • 录用日期：2022-07-08
基金
National Natural Science Foundation of China(82004280)
国家自然科学基金(82004280)
National Natural Science Foundation of China(82074388)
国家自然科学基金(82074388)
作者信息
    1山东中医药大学第一临床医学院，山东济南 250000
    2山东中医药大学附属医院心血管病科，山东济南 250014

通讯作者:

马度芳，E-mail:
参考文献
分享链接
https://castjournals.cast.org.cn/joweb/jfjyxzz/CN/10.11855/j.issn.0577-7402.2023.05.0602
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2种不同金属材料的力学参数
科
Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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