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

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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.

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ERK/MAPK signalling pathway and tumorigenesis

Yan-Jun Guo, Wei-Wei Pan, Sheng-Bing Liu … (2020)

Mitogen-activated protein kinase (MAPK) cascades are key signalling pathways that regulate a wide variety of cellular processes, including proliferation, differentiation, apoptosis and stress responses. The MAPK pathway includes three main kinases, MAPK kinase kinase, MAPK kinase and MAPK, which activate and phosphorylate downstream proteins. The extracellular signal-regulated kinases ERK1 and ERK2 are evolutionarily conserved, ubiquitous serine-threonine kinases that regulate cellular signalling under both normal and pathological conditions. ERK expression is critical for development and their hyperactivation plays a major role in cancer development and progression. The Ras/Raf/MAPK (MEK)/ERK pathway is the most important signalling cascade among all MAPK signal transduction pathways, and plays a crucial role in the survival and development of tumour cells. The present review discusses recent studies on Ras and ERK pathway members. With respect to processes downstream of ERK activation, the role of ERK in tumour proliferation, invasion and metastasis is highlighted, and the role of the ERK/MAPK signalling pathway in tumour extracellular matrix degradation and tumour angiogenesis is emphasised.

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New insights into TGF-β/Smad signaling in tissue fibrosis

Ying-Yong Zhao, He-He Hu, Dan-Qian Chen … (2018)

Transforming growth factor-β1 (TGF-β1) is considered as a crucial mediator in tissue fibrosis and causes tissue scarring largely by activating its downstream small mother against decapentaplegic (Smad) signaling. Different TGF-β signalings play different roles in fibrogenesis. TGF-β1 directly activates Smad signaling which triggers pro-fibrotic gene overexpression. Excessive studies have demonstrated that dysregulation of TGF-β1/Smad pathway was an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulator that promote TGF-β1-mediated tissue fibrosis, while Smad7 serves as a negative feedback regulator of TGF-β1/Smad pathway thereby protects against TGF-β1-mediated fibrosis. This review presents an overview of the molecular mechanisms of TGF-β/Smad signaling pathway in renal, hepatic, pulmonary and cardiac fibrosis, followed by an in-depth discussion of their molecular mechanisms of intervention effects both in vitro and in vivo. The role of TGF-β/Smad signaling pathway in tumor or cancer is also discussed. Additionally, the current advances also highlight targeting TGF-β/Smad signaling pathway for the prevention of tissue fibrosis. The review reveals comprehensive pathophysiological mechanisms of tissue fibrosis. Particular challenges are presented and placed within the context of future applications against tissue fibrosis.

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Idiopathic pulmonary fibrosis

Annie Pardo, Ganesh Raghu, Luca Richeldi … (2017)

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by progressive lung scarring and the histological picture of usual interstitial pneumonia (UIP). It is associated with increasing cough and dyspnoea and impaired quality of life. IPF affects ∼3 million people worldwide, with incidence increasing dramatically with age. The diagnostic approach includes the exclusion of other interstitial lung diseases or overlapping conditions and depends on the identification of the UIP pattern, usually with high-resolution CT; lung biopsy might be required in some patients. The UIP pattern is predominantly bilateral, peripheral and with a basal distribution of reticular changes associated with traction bronchiectasis and clusters of subpleural cystic airspaces. The biological processes underlying IPF are thought to reflect an aberrant reparative response to repetitive alveolar epithelial injury in a genetically susceptible ageing individual, although many questions remain on how to define susceptibility. Substantial progress has been made in the understanding of the clinical management of IPF, with the availability of two pharmacotherapeutic agents, pirfenidone and nintedanib, that decrease physiological progression and likely improve progression-free survival. Current efforts are directed at identifying IPF early, potentially relying on combinations of biomarkers that include circulating factors, demographics and imaging data.

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Journal

Journal ID (nlm-ta): Int J Mol Med

Journal ID (iso-abbrev): Int J Mol Med

Journal ID (publisher-id): IJMM

Title: International Journal of Molecular Medicine

Publisher: D.A. Spandidos

ISSN (Print): 1107-3756

ISSN (Electronic): 1791-244X

Publication date (Print): July 2021

Publication date (Electronic): 18 May 2021

Publication date PMC-release: 18 May 2021

Volume: 48

Issue: 1

Electronic Location Identifier: 132

Affiliations

Department of Pathology, Basic Medical School, Central South University, Changsha, Hunan 410006, P.R. China

Author notes

Correspondence to: Dr Yongbin Hu, Department of Pathology, Basic Medical School, Central South University, 172 Tongzipo Road, Changsha, Hunan 410006, P.R. China, E-mail: yongbinhu@ 123456csu.edu.cn

Article

Publisher ID: ijmm-48-01-04965

DOI: 10.3892/ijmm.2021.4965

PMC ID: 8136122

PubMed ID: 34013369

SO-VID: 3856bfa9-c7f7-4fa5-9381-181e8c2eef89

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

History

Date received : 23 January 2021

Date accepted : 29 April 2021

Funding

Funded by: National Natural Science Foundation of China

Award ID: 81673120

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

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

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International Journal of Medicine and Medical Research

Most cited references 123

ERK/MAPK signalling pathway and tumorigenesis

New insights into TGF-β/Smad signaling in tissue fibrosis

Idiopathic pulmonary fibrosis

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