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特发性肺纤维化中衰老特征的更新

Update of Aging Hallmarks in Idiopathic Pulmonary Fibrosis.

作者信息

Torres-Machorro Ana Lilia, García-Vicente Ángeles, Espina-Ordoñez Marco, Luis-García Erika, Negreros Miguel, Herrera Iliana, Becerril Carina, Toscano Fernanda, Cisneros Jose, Maldonado Mariel

机构信息

Laboratorio de Biología Celular, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.

Facultad de Ciencias, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.

出版信息

Cells. 2025 Feb 5;14(3):222. doi: 10.3390/cells14030222.

DOI:10.3390/cells14030222
PMID:39937013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11817138/
Abstract

Idiopathic Pulmonary Fibrosis (IPF) is an epithelial-driven interstitial lung disease of unknown etiology characterized by the excessive proliferation of fibroblast populations that synthesize large amounts of extracellular matrix. In this devastating disorder, all aging hallmarks appear prematurely or are altered. This review highlights key findings about IPF characteristics recently recognized as hallmarks of aging, including mechanical alterations, inflammaging, dysbiosis, alternative splicing, and disabled macroautophagy. It also revisits the classic hallmarks of aging, which encompass stem cell exhaustion, cellular senescence, and altered intercellular communication. Enhancing our understanding of the fundamental processes that underlie the altered hallmarks of aging in IPF may facilitate the development of innovative experimental strategies to improve therapeutic outcomes.

摘要

特发性肺纤维化(IPF)是一种病因不明的上皮驱动的间质性肺疾病,其特征是成纤维细胞群体过度增殖,合成大量细胞外基质。在这种毁灭性疾病中,所有衰老特征都过早出现或发生改变。本综述重点介绍了最近被认为是衰老特征的IPF特性的关键发现,包括机械改变、炎症衰老、生态失调、可变剪接和自噬功能障碍。它还重新审视了衰老的经典特征,包括干细胞耗竭、细胞衰老和细胞间通讯改变。加强我们对IPF中衰老特征改变所依据的基本过程的理解,可能有助于开发创新的实验策略,以改善治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/6e73d8b97f16/cells-14-00222-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/62aac7371fab/cells-14-00222-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/fd77eeadc135/cells-14-00222-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/8c4112553064/cells-14-00222-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/6e73d8b97f16/cells-14-00222-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/62aac7371fab/cells-14-00222-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/fd77eeadc135/cells-14-00222-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/8c4112553064/cells-14-00222-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0ed/11817138/6e73d8b97f16/cells-14-00222-g004.jpg

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Altered expression pattern of immune response-related genes and isoforms in hypersensitivity pneumonitis lung fibroblasts.免疫反应相关基因和亚型在过敏性肺炎肺成纤维细胞中的表达模式改变。
Sci Rep. 2024 Oct 14;14(1):24002. doi: 10.1038/s41598-024-74267-x.
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Role of telomere dysfunction and immune infiltration in idiopathic pulmonary fibrosis: new insights from bioinformatics analysis.
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Calpain-1 Up-Regulation Promotes Bleomycin-Induced Pulmonary Fibrosis by Activating Ferroptosis.钙蛋白酶-1 上调通过激活铁死亡促进博来霉素诱导的肺纤维化。
Am J Pathol. 2024 Dec;194(12):2272-2289. doi: 10.1016/j.ajpath.2024.09.004. Epub 2024 Sep 24.
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Front Cell Infect Microbiol. 2024 Aug 19;14:1401448. doi: 10.3389/fcimb.2024.1401448. eCollection 2024.
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