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

被引：38

作者：

Effendi, Wiwin Is ^{[1
,2
,3
]}

Nagano, Tatsuya ^{[4
]}

机构：

[1] Univ Airlangga, Fac Med, Dept Pulmonol & Resp Med, Surabaya 60132, Indonesia

[2] Univ Airlangga Teaching Hosp, Dept Pulmonol & Resp Med, Surabaya 60015, Indonesia

[3] Univ Airlangga Teaching Hosp, Pulmonol & Resp Med UNAIR PaRU Res Ctr, Surabaya 60015, Indonesia

[4] Kobe Univ, Dept Internal Med, Div Resp Med, Grad Sch Med,Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo 6500017, Japan

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2022年 / 23卷 / 11期

关键词：

CTGF; pro-fibrotic; mitochondria dysfunction; metabolic dysregulation; senescence; chronic respiratory diseases; idiopathic pulmonary fibrosis; FACTOR CTGF EXPRESSION; ALVEOLAR EPITHELIAL-CELLS; RECEPTOR 5 S1P(5); SPHINGOSINE; 1-PHOSPHATE; EXTRACELLULAR-MATRIX; LYSOPHOSPHATIDIC ACID; LUNG FIBROBLASTS; MYOFIBROBLAST DIFFERENTIATION; MITOCHONDRIAL DYSFUNCTION; MESENCHYMAL TRANSITION;

D O I：

10.3390/ijms23116064

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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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页数：19

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