PCR array analysis reveals a novel expression profile of ferroptosis-related genes in idiopathic pulmonary fibrosis

Table 4 The influence of identified DE-FRGs on pulmonary fibrosis and their potential role in clinical translational application

Gene	Potential role in the clinical translational application of pulmonary fibrosis	Major effect on pulmonary fibrosis (clinical/preclinical findings)	Ref
BBC3	Potential novel therapeutic target for pulmonary fibrosis	Knockdown of BBC3 expression in vitro and in vivo attenuated silica-induced lung fibrosis by reducing autophagy occurrence	[25]
CP	Potential as a serum biomarker of lung fibrosis	Serum levels of CP were significantly correlated with the exposure levels of respirable fibers in occupational exposure-related pulmonary fibrosis	[26]
NOX3	Downstream target of the profibrotic factor IGFBP-5	IGFBP-5 stimulated transcriptional expression of NOX3 in human fibroblasts. Selective knockdown of NOX3 reduced ROS production by IGFBP-5	[27]
TF	Potential biomarker of IPF	BAL fluid from IPF patients had elevated TF levels compared to controls	[28]
EPRS	Potential therapeutic target for anti-IPF interventions	EPRS regulated the expression of mesenchymal markers and extracellular matrix proteins through TGFβ1–STAT signaling in in vitro and in vivo IPF models	[29]
FTH1	Downstream target of potential pulmonary fibrosis therapeutic DHQ	DHQ suppressed ferritinophagy by upregulating FTH1, attenuating silica-induced pulmonary fibrosis in an in vitro model	[30]
SLC39A8	Potential therapeutic target in pulmonary fibrosis	SLC39A8 deficiency reduced AEC2 regeneration and increased lung fibrosis	[31]

IGFBP-5 Insulin-like growth factor binding protein-5, ROS Reactive oxygen species, BAL Bronchoalveolar lavage, DHQ Dihydroquercetin, AEC2 Type 2 alveolar epithelial cells

ISSN: 1471-2466