LEYKOTSIT DISFUNKTSIYASI, ENDOTELIAL SHIKASTLANISH VA YALLIG‘LANISHDAN TOMIR DEVORI QAYTA QURILISHIGACHA BO‘LGAN PATOLOGIK JARAYONLARNING INTEGRATSIYASI

Authors

  • Xalilov Sanjar Abdivohid o'g'li Toshkent Davlat Tibbiyot Universiteti Odam anatomiyasi va OXTA kafedrasi assistenti Author
  • Xalilov Hikmatulla Dilshod o`g`li Toshkent Davlat Tibbiyot Universiteti Normal va patologik fiziologiya kafedrasi assistenti Author
  • Achildiyev Nurbek Elbekovich Toshkent Davlat Tibbiyot Universiteti Stomatologiya fakulteti talabasi Author

Keywords:

Leykotsit disfunktsiyasi, endotelial disfunksiya, yallig‘lanish, vaskulyar remodeling, tomir infiltratsiyasi, sitokinlar, matriks metalloproteinazalar, ateroskleroz, NLRP3 inflammasoma, NF-κB.

Abstract

So‘nggi o‘n yil ichida kardiovaskulyar patologiyalarning molekulyar va hujayraviy mexanizmlarini o‘rganish bo‘yicha olib borilgan tadqiqotlar shuni ko‘rsatdiki, leykotsit disfunktsiyasi, endotelial shikastlanish va yallig‘lanish jarayonlari o‘rtasidagi o‘zaro bog‘liqlik tomir devorining patologik qayta qurilishi (vaskulyar remodeling) va ateroskleroz, arterial gipertenziya, yurak yetishmovchiligi kabi ko‘plab kasalliklarning rivojlanishida markaziy rol o‘ynaydi [1,2]. Bu sharhli maqola 2015-2025-yillarda chop etilgan ilmiy ma’lumotlarni umumlashtirib, ushbu murakkab o‘zaro ta’sir yo‘llarini tizimli tahlil qilishga qaratilgan. Maqolada, birinchi navbatda, monotsitlar, neytrofillar, limfotsitlar va makrofaglarning faollashuvida endotelial disfunksiyaning induksiyalovchi roli, shuningdek, yallig‘lanish sitokinlarining (TNF-α, IL-1β, IL-6) hamda kislorod radikallari va azot oksidining muvozanati buzilishining vazifasi tahlii qilinadi [3,4]. Keyinchalik, yallig‘lanish signallarining tutash nuqtasi sifatida NF-κB va NLRP3 inflammasoma kabi molekulyar yo‘llarning faollashishi va ularning hujayra adezyon molekulalari (VCAM-1, ICAM-1) ifodasini oshirish orqali leykotsitlarning tomir devoriga infiltratsiyasini kuchaytirish mexanizmlari ko‘rib chiqiladi [5,6]. Tomir devorining qayta qurilishining yakuniy bosqichida, makrofaglar tomonidan ishlab chiqariladigan matriks metalloproteinazalar (MMP-2, MMP-9) va o‘sish omillarining (TGF-β, PDGF) faolligining oshishi natijasida silliq mushak hujayralarining migratsiyasi va proliferatsiyasi, shuningdek, ekstrasellyular matriksning to‘planishi kabi hodisalar yuzaga keladi, bu esa tomir qattiqligi va stenozining rivojlanishiga olib keladi [7,8]. Ushbu sharh jarayonlarni boshqarishning yangi terapevtik strategiyalarini ishlab chiqish uchun nazariy asos yaratadi, jumladan, aniq molekulyar nishonlarni blokirovka qilish, leykotsit-endotel o‘zaro ta’sirini modulyatsiya qilish va yallig‘lanishga qarshi yangi yondashuvlarni qo‘llash imkoniyatlarini taqdim etadi [9,10].

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Published

2026-01-01