Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge

CTGF is upregulated in patients with idiopathic pulmonary fibrosis (IPF), characterized by the deposition of a pathological extracellular matrix (ECM). Additionally, many omics studies confirmed that aberrant cellular senescence-associated mitochondria dysfunction and metabolic reprogramming had bee...

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Main Authors: Wiwin Is Effendi, Tatsuya Nagano
Format: Article
Language:English
Published: MDPI AG 2022-05-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/11/6064
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author Wiwin Is Effendi
Tatsuya Nagano
author_facet Wiwin Is Effendi
Tatsuya Nagano
author_sort Wiwin Is Effendi
collection DOAJ
description CTGF is upregulated in patients with idiopathic pulmonary fibrosis (IPF), characterized by the deposition of a pathological extracellular matrix (ECM). Additionally, many omics studies confirmed that aberrant cellular senescence-associated mitochondria dysfunction and metabolic reprogramming had been identified in different IPF lung cells (alveolar epithelial cells, alveolar endothelial cells, fibroblasts, and macrophages). Here, we reviewed the role of the CTGF in IPF lung cells to mediate anomalous senescence-related metabolic mechanisms that support the fibrotic environment in IPF.
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spelling doaj.art-7d19bf6ed24d451887b599c3d59d106e2023-11-23T14:08:59ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-05-012311606410.3390/ijms23116064Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the BridgeWiwin Is Effendi0Tatsuya Nagano1Department of Pulmonology and Respiratory Medicine, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, IndonesiaDivision of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, JapanCTGF is upregulated in patients with idiopathic pulmonary fibrosis (IPF), characterized by the deposition of a pathological extracellular matrix (ECM). Additionally, many omics studies confirmed that aberrant cellular senescence-associated mitochondria dysfunction and metabolic reprogramming had been identified in different IPF lung cells (alveolar epithelial cells, alveolar endothelial cells, fibroblasts, and macrophages). Here, we reviewed the role of the CTGF in IPF lung cells to mediate anomalous senescence-related metabolic mechanisms that support the fibrotic environment in IPF.https://www.mdpi.com/1422-0067/23/11/6064CTGFpro-fibroticmitochondria dysfunctionmetabolic dysregulationsenescencechronic respiratory diseases
spellingShingle Wiwin Is Effendi
Tatsuya Nagano
Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge
International Journal of Molecular Sciences
CTGF
pro-fibrotic
mitochondria dysfunction
metabolic dysregulation
senescence
chronic respiratory diseases
title Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge
title_full Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge
title_fullStr Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge
title_full_unstemmed Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge
title_short Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge
title_sort connective tissue growth factor in idiopathic pulmonary fibrosis breaking the bridge
topic CTGF
pro-fibrotic
mitochondria dysfunction
metabolic dysregulation
senescence
chronic respiratory diseases
url https://www.mdpi.com/1422-0067/23/11/6064
work_keys_str_mv AT wiwiniseffendi connectivetissuegrowthfactorinidiopathicpulmonaryfibrosisbreakingthebridge
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