TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

Int J Mol Med. 2021 Jul;48(1):132. doi: 10.3892/ijmm.2021.4965. Epub 2021 May 20.

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.

Keywords: ERK; MAPK; Smad; TGF‑β1; idiopathic pulmonary fibrosis.

Publication types

  • Review

MeSH terms

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

Substances

  • Apoptosis Regulatory Proteins
  • DIABLO protein, human
  • Mitochondrial Proteins
  • TGFB1 protein, human
  • Transforming Growth Factor beta1

Grants and funding

This review was funded by the National Natural Science Foundation of China (grant no. 81673120).