Downregulation of a potential therapeutic target NPAS2, regulated by p53, alleviates pulmonary fibrosis by inhibiting epithelial-mesenchymal transition via suppressing HES1

Chen, Yingying; He, Zhong; Zhao, Bo; Zheng, Rui

doi:10.1016/j.cellsig.2023.110795

Cited by 2 publications

(1 citation statement)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…AEC-specific activation of p53-miR-34a feedback has been shown to promote pulmonary fibrosis by accelerating AEC apoptosis, while fibroblast-specific activation of p53-miR-34a significantly inhibits pulmonary fibrosis through promoting fibroblast apoptosis and senescence [ 102 , 103 ]. Neuronal PAS domain protein 2 (NPAS2) is a novel target gene of p53, Chen et al revealed that p53 transcriptionally activates NPAS2 to promote EMT of AT2 cells and BLM-mediated pulmonary fibrosis [ 104 ]. Another study also found that activation of p53/RMRP/miR122 feedback loop can activate Notch-dependent EMT to aggravate silica-induce pulmonary fibrosis [ 105 ].…”

Section: Roles Of P53 In Organ Fibrosismentioning

confidence: 99%

Targeting tumor suppressor p53 for organ fibrosis therapy

Bao,

Yang,

Shen

et al. 2024

Cell Death Dis

View full text Add to dashboard Cite

Fibrosis is a reparative and progressive process characterized by abnormal extracellular matrix deposition, contributing to organ dysfunction in chronic diseases. The tumor suppressor p53 (p53), known for its regulatory roles in cell proliferation, apoptosis, aging, and metabolism across diverse tissues, appears to play a pivotal role in aggravating biological processes such as epithelial-mesenchymal transition (EMT), cell apoptosis, and cell senescence. These processes are closely intertwined with the pathogenesis of fibrotic disease. In this review, we briefly introduce the background and specific mechanism of p53, investigate the pathogenesis of fibrosis, and further discuss p53’s relationship and role in fibrosis affecting the kidney, liver, lung, and heart. In summary, targeting p53 represents a promising and innovative therapeutic approach for the prevention and treatment of organ fibrosis.

show abstract