关键词: ERK MAPK Smad TGF‑β1 idiopathic pulmonary fibrosis

Mesh : Apoptosis Regulatory Proteins / genetics metabolism Humans Idiopathic Pulmonary Fibrosis / pathology therapy MAP Kinase Signaling System Mitochondrial Proteins / genetics metabolism Signal Transduction Transforming Growth Factor beta1 / genetics metabolism

来  源:   DOI:10.3892/ijmm.2021.4965   PDF(Pubmed)

Abstract:
Idiopathic pulmonary fibrosis (IPF) is a worldwide disease characterized by the chronic and irreversible decline of lung function. Currently, there is no drug to successfully treat the disease except for lung transplantation. Numerous studies have been devoted to the study of the fibrotic process of IPF and findings showed that transforming growth factor‑β1 (TGF‑β1) plays a central role in the development of IPF. TGF‑β1 promotes the fibrotic process of IPF through various signaling pathways, including the Smad, MAPK, and ERK signaling pathways. There are intersections between these signaling pathways, which provide new targets for researchers to study new drugs. In addition, TGF‑β1 can affect the fibrosis process of IPF by affecting oxidative stress, epigenetics and other aspects. Most of the processes involved in TGF‑β1 promote IPF, but TGF‑β1 can also inhibit it. This review discusses the role of TGF‑β1 in IPF.
摘要:
特发性肺纤维化(IPF)是一种全球性疾病,其特征是肺功能的慢性和不可逆转的下降。目前,除了肺移植,没有药物可以成功治疗这种疾病。许多研究致力于IPF纤维化过程的研究,发现转化生长因子β1(TGFβ1)在IPF的发展中起着核心作用。TGF-β1通过各种信号通路促进IPF的纤维化过程,包括Smad,MAPK,和ERK信号通路。这些信号通路之间有交叉点,这为研究人员研究新药提供了新的靶点。此外,TGF-β1可通过影响氧化应激影响IPF纤维化进程,表观遗传学和其他方面。参与TGF-β1的大多数过程促进IPF,但是TGF-β1也可以抑制它。本文就TGF-β1在IPF中的作用作一综述。
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