ETIOPATHOGENETIC SIGNIFICANCE OF POLYMORPHISMS OF THE IL10, SERPINE1, NOS3, AND IL1Β GENES IN THE DEVELOPMENT OF MAXILLOFACIAL NECROSIS

Boymuradov Sh.A., Kurbanov Y.Kh., Narmurotov B.K., Djurayev J.A.

Вестник Ассоциации пульмонологов Центральной Азии · 2026-yil

Annotatsiya

Maxillofacial purulent-necrotic lesions represent a serious clinical problem due to their aggressive course, high risk of complications, and limited effectiveness of standard therapeutic approaches. In recent years, increasing attention has been paid to the role of genetic factors that determine individual susceptibility to severe inflammatory and necrotic processes in the maxillofacial region. This study focuses on the etiopathogenetic significance of polymorphisms in the IL10, SERPINE1, NOS3, and IL1β genes, which are involved in immune regulation, inflammatory response, vascular function, and tissue perfusion. Variations in the IL10 gene may affect anti-inflammatory cytokine production, leading to prolonged inflammation and impaired tissue repair. Polymorphisms of the SERPINE1 gene are associated with disturbances in fibrinolysis and microcirculation, increasing the risk of ischemia and necrosis. NOS3 gene variants contribute to endothelial dysfunction and reduced nitric oxide synthesis, negatively influencing blood flow and regenerative capacity. IL1β gene polymorphisms enhance pro-inflammatory activity, promoting extensive tissue destruction. The combined effect of these genetic variations plays a significant role in the severity, progression, and clinical outcomes of maxillofacial necrosis. Understanding these mechanisms may improve risk stratification, early diagnosis, and the development of personalized therapeutic strategies.

Maqola ma’lumotlari
MualliflarBoymuradov Sh.A., Kurbanov Y.Kh., Narmurotov B.K., Djurayev J.A.
JurnalВестник Ассоциации пульмонологов Центральной Азии
Nashr sanasi2026-02-11
Jild17
Son12
Betlar23-27
TilRus

Kalit so‘zlar

maxillofacial necrosis, gene polymorphism, IL10, SERPINE1, NOS3, IL1β, inflammation, genetic susceptibility.

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