DNK METILLANISHI BUZILISHLARINING AUTOIMMUN TIREOIDIT PATOGENEZIDAGI O‘RNI
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autoimmun tireoidit, polimorfizm, metillanish, gipometillanish, gomotsistein, gipergomotsisteinemiya, gipotiroidizm, eutireoz##article.abstract##
Autoimmun tireoidit (AIT) qalqonsimon bezning eng keng tarqalgan autoimmun kasalliklaridan biri bo‘lib, u genetik, atrof-muhit va epigenetik omillarning murakkab o‘zaro ta’siri natijasida shakllanadi. So‘nggi yillarda DNK metillanishi buzilishlariga alohida e’tibor qaratilmoqda, u folat almashinuvi va gomotsistein metabolizmi bilan uzviy bog‘liq bo‘lib, mazkur jarayonning asosiy fermenti metilentrofolat reduktaza (MTHFR) hisoblanadi. Ushbu sharhning maqsadi AIT patogenezida MTHFR geni polimorfizmlari hamda ular bilan bog‘liq epigenetik va metabolik buzilishlarning rolini tahlil qilishdan iborat. Sharh yetakchi xalqaro ma’lumotlar bazalarida chop etilgan tizimli sharhlar, meta-tahlillar va original klinik-laborator tadqiqotlar ma’lumotlariga asoslangan. AITda DNKning global gipometillanishi va immunoregulyator genlar, jumladan NOTCH1, HLA-DRB1, TNF va ICAM1 genlarida metillanishning differensial o‘zgarishlari aniqlangan. MTHFR C677T va A1298C polimorfizmlari ferment faolligining o‘zgarishi, gomotsistein darajasining oshishi va gipotiroidizm rivojlanish xavfi bilan bog‘liq. Shuningdek, gipergomotsisteinemiya, folatlar va B guruhi vitaminlari tanqisligi, shuningdek, eutireoid bemorlarda tireotrop gormon (TTG) darajasining oshishi va AT-TPO ning ijobiyligi AITdagi erta metabolik va epigenetik siljishlarning o‘zaro bog‘liq bo‘g‘inlari bo‘lishi mumkinligi ko‘rsatilgan. Olingan natijalar AIT patogenezida metillanish buzilishlarining potensial rolini tasdiqlaydi, biroq sabab-oqibat bog‘liqligini aniqlash uchun qo‘shimcha prospektiv tadqiqotlar zarur.
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