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Copied from pulmonary fibrosis {[p53 is a tumor suppressor protein that plays a critical role in regulating cell cycle progression and preventing the development of cancer. In addition to its role in cancer prevention, emerging evidence suggests that p53 may also play a role in the development of pulmonary fibrosis.

Studies have shown that p53 expression is increased in lung tissue from patients with pulmonary fibrosis. Animal models of pulmonary fibrosis have also demonstrated that increased p53 activity is associated with the development and progression of the disease.

One proposed mechanism by which p53 may contribute to the development of pulmonary fibrosis is through the regulation of cellular senescence. Cellular senescence is a process by which cells stop dividing and enter a state of growth arrest, and it has been implicated in the development of various age-related diseases, including pulmonary fibrosis. Studies have shown that p53 can induce cellular senescence in lung fibroblasts, which are the cells responsible for the production of extracellular matrix proteins that contribute to the development of pulmonary fibrosis.]}

Commonly knonw molecules implaicted in fibrosis are Transforming Growth Factor-Beta (TGF-β), Connective Tissue Growth Factor (CTGF), Epidermal Growth Factor Receptor (EGFR), Interleukin-13 (IL-13),Platelet-Derived Growth Factor (PDGF),Wnt/β-catenin signaling pathway. TGF-β is a cytokine that plays a critical role in the regulation of ECM production and cellular differentiation. It is a potent stimulator of fibrosis, and increased TGF-β signaling is associated with the development of fibrosis in various organs. CTGF is a matricellular protein that is involved in ECM production and remodeling. It is upregulated in response to TGF-β and has been implicated in the development of pulmonary fibrosis. EGFR is a transmembrane receptor that plays a role in cellular proliferation, differentiation, and survival. Dysregulated EGFR signaling has been implicated in the development of pulmonary fibrosis, and drugs that target EGFR have been shown to have therapeutic potential in the treatment of the disease. IL-13 is a cytokine that is involved in the regulation of immune responses. It has been shown to promote fibrosis in the lungs by stimulating the production of ECM proteins and the recruitment of fibroblasts to sites of tissue injury. PDGF is a cytokine that plays a key role in the regulation of cell proliferation and migration. It is involved in the recruitment of fibroblasts to sites of tissue injury in the lungs, and increased PDGF signaling is associated with the development and progression of pulmonary fibrosis. Wnt/β-catenin signaling plays a critical role in tissue repair and regeneration, and dysregulated Wnt/β-catenin signaling has been implicated in the development of pulmonary fibrosis.

Saito, A., Horie, M., & Nagase, T. (2018). TGF-β Signaling in Lung Health and Disease. International journal of molecular sciences, 19(8), 2460. https://doi.org/10.3390/ijms19082460

Yang, J., Velikoff, M., Canalis, E., Horowitz, J. C., & Kim, K. K. (2014). Activated alveolar epithelial cells initiate fibrosis through autocrine and paracrine secretion of connective tissue growth factor. ''American journal of physiology. Lung cellular and molecular physiology, 306''(8), L786–L796. https://doi.org/10.1152/ajplung.00243.2013

Liu, J., Xiao, Q., Xiao, J., Niu, C., Li, Y., Zhang, X., Zhou, Z., Shu, G., & Yin, G. (2022). Wnt/β-catenin signalling: function, biological mechanisms, and therapeutic opportunities. Signal transduction and targeted therapy, 7(1), 3. https://doi.org/10.1038/s41392-021-00762-6

Andrae, J., Gallini, R., & Betsholtz, C. (2008). Role of platelet-derived growth factors in physiology and medicine. Genes & development, 22(10), 1276–1312. https://doi.org/10.1101/gad.1653708

Ojo, A. S., Balogun, S. A., Williams, O. T., & Ojo, O. S. (2020). Pulmonary Fibrosis in COVID-19 Survivors: Predictive Factors and Risk Reduction Strategies. Pulmonary medicine, 2020, 6175964. https://doi.org/10.1155/2020/6175964

Todd, N. W., Luzina, I. G., & Atamas, S. P. (2012). Molecular and cellular mechanisms of pulmonary fibrosis. Fibrogenesis & tissue repair, 5(1), 11. https://doi.org/10.1186/1755-1536-5-11