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

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MDPI
DOI: 10.3390/ijms23116064

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CTGF; pro-fibrotic; mitochondria dysfunction; metabolic dysregulation; senescence; chronic respiratory diseases; idiopathic pulmonary fibrosis

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In this review, we explored the role of CTGF in IPF lung cells in mediating abnormal aging-related metabolic mechanisms that contribute to the fibrotic environment in IPF.
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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