PROTON-SEZUVCHI RETSEPTORLAR (GPR65, TDAG8) ORQALI PH-SIGNAL TRANSDUKSIYASI VA NEYTROFIL FENOTIPINING SHAKLLANISHI. PATOFIZIOLOGIK AHAMIYAT VA TERAPEVTIK ISTIQBOLLAR
Keywords:
GPR65, TDAG8, proton-sezuvchi retseptorlar, pH-signal, neytrofil fenotipi, yallig'lanish, asidoz, neytrofil apoptozi, yallig'lanishli ichak kasalliklari, cAMP signal yo'li [1, 4, 7].Abstract
So'nggi o'n yillikdagi tadqiqotlar to'qima mikromuhitidagi pH o'zgarishlari nafaqat patologik jarayonlarning passiv natijasi, balki immun javobni faol tartibga soluvchi muhim signal mexanizmi ekanligini ko'rsatdi. Hujayradan tashqari muhitning kislotalashuvi (asidoz) yallig'lanish, ishemiya, o'sma o'sishi va autoimmun kasalliklarning ajralmas xususiyati hisoblanadi. Organizmda pH o'zgarishlarini sezish uchun ixtisoslashgan bir qancha sensor tizimlar mavjud bo'lib, ulardan eng muhimlaridan biri bu proton-sezuvchi G-oqsil bilan bog'langan retseptorlar (GPCRlar) oilasidir. Ushbu oilaning vakillari — GPR4, GPR68 (OGR1) va GPR65 (TDAG8) — hujayradan tashqari pH ning fiziologik (7.4) va patologik (6.5–6.8) oralig'idagi o'zgarishlariga javob beradi. Mazkur maqolada, asosiy e'tibor GPR65/TDAG8 retseptorining neytrofil fenotipi va funksiyasini shakllantirishdagi o'rni hamda uning yallig'lanish kasalliklaridagi patofiziologik ahamiyatiga qaratilgan. TDAG8 asosan gematopoetik hujayralarda, xususan, makrofaglar va neytrofillarda yuqori darajada ifodalanadi va asosan Gs oqsili orqali signal uzatib, hujayra ichidagi siklik adenozin monofosfat (cAMP) darajasini oshiradi. So'nggi tadqiqotlar shuni korsatadiki, TDAG8 yallig'lanish muhitidagi kislotali stimulni qabul qilib, neytrofillarning yashash davomiyligi, apoptozga chidamliligi, migratsiya faolligi va sitokin ishlab chiqarish qobiliyatini modulyatsiya qiladi. Ayniqsa, TDAG8 orqali amalga oshadigan signal yo'li neytrofillarning yallig'lanish o'chog'ida uzoq vaqt yashab qolishi va to'qimalarni shikastlashi mumkin bo'lgan "sitotoksik" fenotipdan, yallig'lanishni cheklovchi va to'qima gomeostazini tiklovchi "regulyator" fenotipga o'tishida muhim rol o'ynashi aniqlangan. Ushbu maqolada, 2015–2025-yillar oralig'ida nashr etilgan ilmiy tadqiqotlar asosida, TDAG8 retseptorining molekulyar mexanizmlari, uning neytrofil biologiyasidagi o'rni va yallig'lanishli ichak kasalliklari (YIK), o'pka kasalliklari hamda neyroyallig'lanishdagi roli batafsil muhokama qilinadi. Shuningdek, TDAG8 ni terapevtik maqsadda qo'llash istiqbollari va bu boradagi muammolar tahlil qilinadi. Ushbu sohadagi bilimlarning chuqurlashishi, yallig'lanish kasalliklarini davolashda yangi strategiyalarni ishlab chiqishga xizmat qilishi mumkin [1, 4, 5].
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