TGF-Β1 GENINING C-509T VA T869C POLIMORFIZMLARINI TIZIMLI SKLERODERMIYADA FIBROZ JARAYONINING GENETIK BIOMARKERLARI SIFATIDA BAHOLASH
Kalit so‘zlar:
tizimli sklerodermiya, TGF-β1 geni, C-509T, T869C, fibrozAbstrak
Tizimli sklerodermiya biriktiruvchi to‘qimaning surunkali autoimmun kasalligi bo‘lib, uning asosiy patogenetik belgilaridan biri teri va ichki a’zolarda fibroz jarayonining rivojlanishidir. Fibrozning shakllanishida transformatsiyalovchi o‘sish omili beta-1 (TGF-β1) muhim rol o‘ynaydi. Ushbu tadqiqotning maqsadi TGF-β1 genining C-509T (rs1800469) va T869C (rs1800470) polimorfizmlarini tizimli sklerodermiyada fibroz jarayonining genetik biomarkerlari sifatida baholashdan iborat bo‘ldi. Tadqiqot holat–nazorat dizaynida olib borildi. Genetik tahlillar real vaqt rejimidagi polimeraza zanjir reaksiyasi yordamida amalga oshirildi. Olingan natijalar T869C polimorfizmining ayrim genotiplari va allellari fibroz rivojlanishi hamda TGF-β1 ekspressiyasi bilan bog‘liq bo‘lishi mumkinligini ko‘rsatdi. C-509T polimorfizmi esa ayrim laborator ko‘rsatkichlar bilan bog‘liqlik namoyon etgan bo‘lsa-da, uning kasallikka moyillikdagi ahamiyati nisbatan past bo‘ldi. Tadqiqot natijalari TGF-β1 genining polimorfizmlarini tizimli sklerodermiyada fibroz rivojlanishini prognozlash, kasallik faolligini baholash va individual davolash strategiyalarini ishlab chiqishda qo‘llash istiqbollarini ko‘rsatadi.
##plugins.themes.default.displayStats.downloads##
Havolalar
1. Allanore, Y., Simms, R., Distler, O., Trojanowska, M., Pope, J., Denton, C. P., & Varga, J. (2015). Systemic sclerosis. Nature Reviews Disease Primers, 1, 15002. https://doi.org/10.1038/nrdp.2015.2
2. Asano, Y. (2018). The pathogenesis of systemic sclerosis: An understanding based on a common pathologic cascade across multiple organs and additional organ-specific pathologies. Journal of Clinical Medicine, 7(7), 166. https://doi.org/10.3390/jcm7070166
3. Denton, C. P., Khanna, D. (2017). Systemic sclerosis. The Lancet, 390(10103), 1685–1699. https://doi.org/10.1016/S0140-6736(17)30933-9
4. Distler, J. H. W., Györfi, A. H., Ramanujam, M., Whitfield, M. L., Königshoff, M., & Lafyatis, R. (2019). Shared and distinct mechanisms of fibrosis. Nature Reviews Rheumatology, 15(12), 705–730. https://doi.org/10.1038/s41584-019-0322-7
5. Gu, Y. Y., Wang, H., & Wang, Y. (2015). TGF-β1 C-509T and T869C polymorphisms and cancer risk: A meta-analysis. International Journal of Clinical and Experimental Medicine, 8(10), 17932–17940.
6. Krieg, T., Takehara, K. (2020). Skin disease: A cardinal feature of systemic sclerosis. Rheumatology, 59(Suppl. 5), v39–v45. https://doi.org/10.1093/rheumatology/keaa448
7. Lafyatis, R. (2014). Transforming growth factor β—At the centre of systemic sclerosis. Nature Reviews Rheumatology, 10(12), 706–719. https://doi.org/10.1038/nrrheum.2014.137
8. Qu, Y., Zhou, B., Yang, J., Shu, Y., Zhang, X., & Zhao, D. (2019). Association between TGF-β1 polymorphisms and head and neck cancer susceptibility: A meta-analysis. Medicine, 98(30), e16580. https://doi.org/10.1097/MD.0000000000016580
9. Rodríguez-Carrio, J., López, P., Suárez, A. (2021). Biomarkers in systemic sclerosis: Current perspectives and future directions. Frontiers in Immunology, 12, 686660. https://doi.org/10.3389/fimmu.2021.686660
10. Roozbehkia, M., Mahmoudi, M., Jamshidi, A. R., & Nicknam, M. H. (2020). Genetic susceptibility markers in systemic sclerosis: A review. Autoimmunity Reviews, 19(11), 102658. https://doi.org/10.1016/j.autrev.2020.102658
11. Stadtlober, N. P., de Carvalho, J. F., Simão, A. N. C., Dichi, I., & Reiche, E. M. V. (2021). TGFB1 +869T>C (rs1800470) variant is independently associated with susceptibility, laboratory activity and TGF-β1 levels in systemic lupus erythematosus. Autoimmunity, 54(6), 337–345. https://doi.org/10.1080/08916934.2021.1958264
12. Trojanowska, M. (2018). Cellular and molecular aspects of vascular dysfunction in systemic sclerosis. Nature Reviews Rheumatology, 14(8), 453–460. https://doi.org/10.1038/s41584-018-0034-z
13. Varga, J., & Abraham, D. (2007). Systemic sclerosis: A prototypic multisystem fibrotic disorder. Journal of Clinical Investigation, 117(3), 557–567. https://doi.org/10.1172/JCI31139
14. Wu, M., Melichian, D. S., de la Garza, M., Gruner, K., Bhattacharyya, S., Barr, L., & Varga, J. (2019). Rosiglitazone abrogates bleomycin-induced scleroderma and blocks profibrotic responses through regulation of TGF-β signaling. Arthritis & Rheumatology, 71(8), 1408–1418. https://doi.org/10.1002/art.40868
15. Zheng, B., Zhang, J., & Chen, H. (2022). The role of TGF-β signaling pathway in fibrosis-related autoimmune diseases. Frontiers in Immunology, 13, 845367. https://doi.org/10.3389/fimmu.2022.845367
