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Telomere Dysfunction in Idiopathic Pulmonary Fibrosis: A Comprehensive Review
- 1 Shijiazhuang New Channel NO. 25 High School, Shijiazhuang, 050000
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Abstract
Telomere dysfunction has emerged as a critical determinant in the pathogenesis of various diseases, particularly in age-related disorders such as idiopathic pulmonary fibrosis (IPF). This review delves into the telomere hypothesis, elucidating the function and composition of telomeres, while also acknowledging their intricate relationship with cancer, albeit not as the primary focus. This study employs a comprehensive literature review approach to elucidate the mechanisms linking telomere dysfunction to IPF. The review focuses on the genetic mutations associated with telomere shortening, the role of cellular senescence, and the potential of telomerase activation and TGF-β pathway modulation. Telomere dysfunction is a pivotal determinant in the pathogenesis of IPF, providing new insights into disease etiology and therapeutic targets. The intricate interplay between telomere shortening, cellular senescence, inflammation, and fibrosis underscores the complexity of IPF and highlights the need for multifaceted therapeutic approaches. Future research should focus on elucidating the molecular mechanisms underlying telomere dysfunction in IPF, identifying novel biomarkers for early disease detection, and developing safe and effective telomere-targeted therapies.
Keywords
Telomere dysfunction, Idiopathic pulmonary fibrosis, Telomere hypothesis, Cancer, Telomere length, Genetic mutations
[1]. Blackburn, E. H. (2001). Telomeres and telomerase: their mechanisms of action and the effects of altering their functions. FEBS Letters, 502(1-2), 74-78. doi: 10.1016/s0014-5793(01)02778-x
[2]. Olovnikov, A. M. (1973). A theory of marginotomy. The incomplete copying of template margin in enzymatic synthesis of polynucleotides and biological significance of the phenomenon. Journal of Theoretical Biology, 41(1), 181-190. doi: 10.1016/0022-5193(73)90178-6
[3]. de Lange, T. (2005). Shelterin: the protein complex that shapes and safeguards human telomeres. Genes & Development, 19(18), 2100-2110. doi: 10.1101/gad.1346805
[4]. Greider, C. W., & Blackburn, E. H. (1985). Identification of a specific telomere terminal transferase activity in Tetrahymena extracts. Cell, 43(2), 405-413. doi: 10.1016/0092-8674(85)90170-9
[5]. Artandi, S. E., & DePinho, R. A. (2010). Telomeres and telomerase in cancer. Carcinogenesis, 31(1), 9-18. doi: 10.1093/carcin/bgp264
[6]. Henson, J. D., Neumann, A. A., Yeager, T. R., & Reddel, R. R. (2002). Alternative lengthening of telomeres in mammalian cells. Oncogene, 21(4), 598-610. doi: 10.1038/sj.onc.1205070
[7]. Raghu, G., Remy-Jardin, M., Myers, J. L., Richeldi, L., Ryerson, C. J., Lederer, D. J., ... & Collard, H. R. (2018). Diagnosis of idiopathic pulmonary fibrosis. An official ATS/ERS/JRS/ALAT clinical practice guideline. American Journal of Respiratory and Critical Care Medicine, 198(5), e44-e68. doi: 10.1164/rccm.201807-1255ST
[8]. Armanios, M. Y., & Chen, J. J. (2009). Telomeres and idiopathic pulmonary fibrosis. Chest, 136(5), 1364-1370. doi: 10.1378/chest.09-0601
[9]. Zhang, K., Xu, L., & Cong, Y.-S. (2021). Telomere Dysfunction in Idiopathic Pulmonary Fibrosis. Frontiers in Medicine, 8, 739810. doi: 10.3389/fmed.2021.739810
[10]. Selman, M., & Pardo, A. (2002). Role of epithelial cells in idiopathic pulmonary fibrosis: from innocent targets to serial killers. Proceedings of the American Thoracic Society, 1(4), 364-372. doi: 10
[11]. Zhang, Y., Liu, J., Zheng, R., Hou, K., Zhang, Y., Jia, T., ... & Liu, J. (2024). Curcumin analogue EF24 prevents alveolar epithelial cell senescence to ameliorate idiopathic pulmonary fibrosis via activation of PTEN. Phytomedicine, 133, 155882.
[12]. Xu, Y., Lan, P., & Wang, T. (2023). The role of immune cells in the pathogenesis of idiopathic pulmonary fibrosis. Medicina, 59(11), 1984.
[13]. Bao, Y. N., Yang, Q., Shen, X. L., Yu, W. K., Zhou, L., Zhu, Q. R., ... & Cao, G. (2024). Targeting tumor suppressor p53 for organ fibrosis therapy. Cell Death & Disease, 15(5), 336.
[14]. Budi, E. H., Schaub, J. R., Decaris, M., Turner, S., & Derynck, R. (2021). TGF‐β as a driver of fibrosis: physiological roles and therapeutic opportunities. The Journal of pathology, 254(4), 358-373.
Cite this article
Yan,R. (2025). Telomere Dysfunction in Idiopathic Pulmonary Fibrosis: A Comprehensive Review. Theoretical and Natural Science,96,61-65.
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The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.
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Volume title: Proceedings of the 5th International Conference on Biological Engineering and Medical Science
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