• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

炎症和纤维化。

Inflammation and fibrosis.

机构信息

Department of Nephrology, University Hospital Regensburg, Regensburg, Germany.

出版信息

Matrix Biol. 2018 Aug;68-69:106-121. doi: 10.1016/j.matbio.2017.11.010. Epub 2017 Nov 28.

DOI:10.1016/j.matbio.2017.11.010
PMID:29196207
Abstract

Tissue damage and inflammation are important triggers for regeneration and fibrosis. Tissue damage not only induces inflammation in general, it also determines the type and polarization of inflammation by recruiting and activating a variety of different cells types of the innate and adaptive immune system. This review focuses on the pathways leading from tissue damage to inflammation, from inflammation to fibrosis and from fibrosis to function. It covers the pro- and antifibrotic properties of immunological mediators released from T cells, monocytes/macrophages, innate lymphoid cells, basophils and eosinophils and takes into account that extracellular matrix proteins are not only produced by mesenchymal fibroblasts but also by other cell types, especially infiltrating hematopoietic cells. The special requirements for activation and recruitment of these so called fibrocytes are described in detail.

摘要

组织损伤和炎症是再生和纤维化的重要触发因素。组织损伤不仅普遍引发炎症,还通过招募和激活先天和适应性免疫系统的各种不同细胞类型来决定炎症的类型和极化。本综述重点关注从组织损伤到炎症、从炎症到纤维化以及从纤维化到功能的途径。它涵盖了 T 细胞、单核细胞/巨噬细胞、固有淋巴细胞、嗜碱性粒细胞和嗜酸性粒细胞释放的免疫介质的促纤维化和抗纤维化特性,并考虑到细胞外基质蛋白不仅由间充质成纤维细胞产生,而且还由其他细胞类型产生,特别是浸润的造血细胞。详细描述了这些所谓的纤维细胞的激活和募集的特殊要求。

相似文献

1
Inflammation and fibrosis.炎症和纤维化。
Matrix Biol. 2018 Aug;68-69:106-121. doi: 10.1016/j.matbio.2017.11.010. Epub 2017 Nov 28.
2
CCR2 contributes to the recruitment of monocytes and leads to kidney inflammation and fibrosis development.CCR2 有助于单核细胞的募集,并导致肾脏炎症和纤维化的发展。
Inflammopharmacology. 2018 Apr;26(2):403-411. doi: 10.1007/s10787-017-0317-4. Epub 2017 Feb 6.
3
Role of Cardiac Macrophages on Cardiac Inflammation, Fibrosis and Tissue Repair.心脏巨噬细胞在心脏炎症、纤维化和组织修复中的作用。
Cells. 2020 Dec 31;10(1):51. doi: 10.3390/cells10010051.
4
Innate Immune Cytokines, Fibroblast Phenotypes, and Regulation of Extracellular Matrix in Lung.肺中的固有免疫细胞因子、成纤维细胞表型及细胞外基质的调控
J Interferon Cytokine Res. 2017 Feb;37(2):52-61. doi: 10.1089/jir.2016.0112. Epub 2017 Jan 24.
5
Mast cells as effector cells of innate immunity and regulators of adaptive immunity.肥大细胞作为固有免疫的效应细胞和适应性免疫的调节细胞。
Immunol Lett. 2016 Oct;178:10-4. doi: 10.1016/j.imlet.2016.07.003. Epub 2016 Jul 5.
6
Sensory neuron-derived TAFA4 promotes macrophage tissue repair functions.感觉神经元衍生的 TAFA4 促进巨噬细胞的组织修复功能。
Nature. 2021 Jun;594(7861):94-99. doi: 10.1038/s41586-021-03563-7. Epub 2021 May 19.
7
Inflammation, fibrosis and skeletal muscle regeneration in LGMDR9 are orchestrated by macrophages.LGMDR9中的炎症、纤维化和骨骼肌再生由巨噬细胞协调调控。
Neuropathol Appl Neurobiol. 2021 Oct;47(6):856-866. doi: 10.1111/nan.12730. Epub 2021 May 28.
8
N-terminal fragment of cardiac myosin binding protein-C triggers pro-inflammatory responses in vitro.心肌肌球蛋白结合蛋白C的N端片段在体外引发促炎反应。
J Mol Cell Cardiol. 2016 Oct;99:47-56. doi: 10.1016/j.yjmcc.2016.09.003. Epub 2016 Sep 8.
9
Secondary lymphoid tissue chemokine (SLC/CCL21)/CCR7 signaling regulates fibrocytes in renal fibrosis.次级淋巴组织趋化因子(SLC/CCL21)/CCR7信号通路调控肾纤维化中的纤维细胞。
Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14098-103. doi: 10.1073/pnas.0511200103. Epub 2006 Sep 11.
10
Absence of nicotinic acetylcholine receptor α7 subunit amplifies inflammation and accelerates onset of fibrosis: an inflammatory kidney model.烟碱型乙酰胆碱受体α7亚基缺失会加剧炎症并加速纤维化的发生:一种炎症性肾脏模型。
FASEB J. 2015 Aug;29(8):3558-70. doi: 10.1096/fj.14-262493. Epub 2015 May 18.

引用本文的文献

1
Dexamethasone-eluting cochlear implants reduce inflammation and foreign body response in human and murine cochleae.地塞米松洗脱型人工耳蜗可减轻人和小鼠耳蜗的炎症及异物反应。
Sci Rep. 2025 Aug 20;15(1):30615. doi: 10.1038/s41598-025-10739-y.
2
Advances in cGAS-STING Signaling in Fibrosis Diseases: Therapeutic Target in Pathological Scars.纤维化疾病中cGAS-STING信号通路的进展:病理性瘢痕的治疗靶点
J Inflamm Res. 2025 Aug 9;18:10777-10793. doi: 10.2147/JIR.S541656. eCollection 2025.
3
The Characterization of the Neuroimmune Response in Primary Pterygia.
原发性翼状胬肉神经免疫反应的特征
Int J Mol Sci. 2025 Aug 1;26(15):7417. doi: 10.3390/ijms26157417.
4
Drugs Used in the Treatment of Viral Infections for the Prevention of Airway Remodeling in Asthma.用于治疗病毒感染以预防哮喘气道重塑的药物。
Mediators Inflamm. 2025 Jul 24;2025:5526526. doi: 10.1155/mi/5526526. eCollection 2025.
5
Comprehensive analysis of keloid super-enhancer networks reveals FOXP1-mediated anti-senescence mechanisms in fibrosis.瘢痕疙瘩超级增强子网络的综合分析揭示了FOXP1介导的纤维化抗衰老机制。
Cell Mol Biol Lett. 2025 Jul 23;30(1):88. doi: 10.1186/s11658-025-00763-1.
6
Methods for Mitochondrial DNA Damage and Depletion in Immortalized Trabecular Meshwork Cells.永生化小梁网细胞中线粒体DNA损伤与耗竭的方法
Int J Mol Sci. 2025 Jun 28;26(13):6255. doi: 10.3390/ijms26136255.
7
Celastrol alleviates esophageal stricture in rats by inhibiting NLR family pyrin domain containing 3 activation.雷公藤红素通过抑制含NLR家族吡啶结构域蛋白3激活来减轻大鼠食管狭窄。
World J Gastroenterol. 2025 Jun 21;31(23):106949. doi: 10.3748/wjg.v31.i23.106949.
8
Polydatin-curcumin formulation alleviates CTD-ILD-like lung injury in mice via GABBR/PI3K/AKT/TGF-β pathway.虎杖苷-姜黄素制剂通过GABBR/PI3K/AKT/TGF-β途径减轻小鼠CTD-ILD样肺损伤。
Front Pharmacol. 2025 Jun 5;16:1573525. doi: 10.3389/fphar.2025.1573525. eCollection 2025.
9
Panaxatriol saponins exert anti-renal fibrosis by suppressing TNF-α mediated inflammation and TGF-β1/Smad3 signaling pathway.人参三醇皂苷通过抑制肿瘤坏死因子-α介导的炎症和转化生长因子-β1/ Smad3信号通路发挥抗肾纤维化作用。
Ren Fail. 2025 Dec;47(1):2516774. doi: 10.1080/0886022X.2025.2516774. Epub 2025 Jun 19.
10
Soft tissue calcifications in chronic kidney disease-beyond the vasculature.慢性肾脏病中的软组织钙化——血管系统之外
Pflugers Arch. 2025 Jun 5. doi: 10.1007/s00424-025-03098-0.