Jild 3 № 1 (2026): Yanvar - Mart
58-65
2026-03-29
Ochiq kirish

O'tkir miokard infarktida SGLT-2 ingibitorlarini qo'llanishi

Sayyora Z.Aliyeva
Nigora Z.Srojidinova
https://doi.org/10.70626/cardiouz-2026-3-00078

Qabul qilingan: 2026-07-04

Nashr etilgan: 2026-03-29

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Annotatsiya

Kardiorenometabolik sindrom (KRMS) yurak-qon tomir, buyrak va metabolik tizimlar o'rtasidagi murakkab va o'zaro bog'liq patobiologik jarayonlarni aks ettiruvchi ko'p komponentli klinik holat bo'lib, uning markazida visseral adipositet, insulinrezistentlik, adipokinlar disbalansi, surunkali past darajali yallig'lanish (metaflammatsiya) hamda oksidlovchi stress yotadi \cite{1, 2}. Ushbu patologik fon endotelial disfunksiya, azot oksidi (NO) bioyetishmovchiligi, mikrovaskulyar perfuziyaning buzilishi va aterosklerotik blyashkalarning beqarorlashuvi orqali o'tkir miokard infarkti (O'MI) rivojlanishiga olib keladi. KRMS sharoitida rivojlangan O'MI klassik ishemik modeldan farq qilib, nafaqat koronar qon oqimining buzilishi, balki kuchli yallig'lanish javobi, immun tizimning faollashuvi va hujayraviy energetika disbalansi bilan kechadi. Infarktning dastlabki bosqichida DAMPs (damage-associated molecular patterns) orqali Toll-like retseptorlar faollashib, NF-κB signal yo'li ishga tushadi va proinflamator sitokinlar (IL-1β, IL-6, TNF-α) ishlab chiqarilishi ortadi.  Bundan tashqari, mitoxondrial disfunksiya va reaktiv kislorod shakllari (ROS) ning ortiqcha hosil bo'lishi oksidlovchi stressni kuchaytirib, lipidlar peroksidatsiyasi, DNK shikastlanishi va kardiomiosit apoptozini rag'batlantiradi.  So'nggi yillarda natriy-glyukoza kotransporter-2 (SGLT2) ingibitorlari, xususan dapagliflozin, keng qamrovli kardiorenometabolik ta'sirga ega preparatlar sifatida alohida e'tibor qozonmoqda. Ularning terapevtik ta'siri ko'p darajali va kompleks xarakterga ega bo'lib, faqat glyukemik nazorat bilan cheklanmaydi. SGLT2 ingibitorlari yallig'lanish signal yo'llarini (NF-κB, NLRP3 inflammasoma) ingibitsiya qilish, oksidlovchi stressni kamaytirish, mitoxondrial funksiyani tiklash, natriy-vodorod almashinuvi (NHE1) ni susaytirish va hujayra ichidagi kaltsiy ortiqcha yuklanishini kamaytirish orqali kardiomiositlarni himoya qiladi \cite{9, 12}. Mazkur maqolada SGLT2 ingibitorlarining O'MI patogenezidagi o'rni, ularning molekulyar, hujayraviy va tizimli ta'sir mexanizmlari hamda zamonaviy klinik tadqiqotlar (DAPA-MI - Dapagliflozin in Myocardial Infarction) natijalari asosida ularning kardiorenometabolik samaradorligi tizimli ravishda tahlil qilinadi.

Kalit so‘zlar

Adabiyotlar ro'yxati

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Mualliflar haqida

Sayyora Z.Aliyeva
aliyevasayyora150594@gmail.com
Respublika ixtisoslashtirilgan kardiologiya ilmiy-amaliy tibbiyot markazi
Nigora Z.Srojidinova
nigora5505@gmail.com
Respublika ixtisoslashtirilgan kardiologiya ilmiy-amaliy tibbiyot markazi

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Qanday iqtibos keltirish kerak

O’tkir miokard infarktida SGLT-2 ingibitorlarini qo’llanishi (S. Aliyeva & N. Srojidinova, Trans.). (2026). O’ZBEKISTON KARDIOLOGIYASI, 3(1), 58-65. https://doi.org/10.70626/cardiouz-2026-3-00078
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