Doktor axborotnomasi 2026, №2 (123)


Subject of the article

ROLE OF THE AGT GENE IN THE DEVELOPMENT OF CHRONIC KIDNEY DISEASE (138-141)

Authors

I. Sh. Bobojonov

Institution

Tashkent state medical university, Tashkent, Uzbekistan

Abstract

Chronic kidney disease (CKD) is a progressive disorder characterized by gradual loss of renal function and structural damage to kidney tissue. Genetic and environmental factors both contribute to CKD development and pro gression. Among genetic determinants, the angiotensinogen (AGT) gene plays a critical role in regulating the renin angiotensin–aldosterone system (RAAS), which is essential for maintaining blood pressure, fluid balance, and renal hemodynamics. Variations in the AGT gene, particularly the M235T polymorphism, have been associated with in creased angiotensinogen levels and enhanced RAAS activation, contributing to hypertension, glomerular hyperfiltra tion, and progressive renal damage. Overactivation of RAAS leads to increased intraglomerular pressure, inflamma tion, oxidative stress, and fibrosis, ultimately accelerating CKD progression. Additionally, angiotensin II stimulates transforming growth factor-β (TGF-β) expression, promoting extracellular matrix accumulation and renal fibrosis. Understanding the molecular mechanisms linking AGT gene polymorphisms to CKD pathogenesis may provide new insights into personalized therapeutic approaches and early risk assessment. This review summarizes current knowledge on the biological role of the AGT gene, its polymorphisms, and their contribution to the development and progression of chronic kidney disease.

Key words

AGT gene, angiotensinogen, chronic kidney disease, renin–angiotensin system, genetic polymorphism, renal fibrosis, hypertension

Literature

1. Bikbov, B., et al. (2020). Global, regional, and national burden of chronic kidney disease, 1990–2017. The Lancet, 395(10225), 709–733. 2. Kim, H. S., et al. (2015). The role of the renin–angiotensin system in kidney disease. Kidney Research and Clinical Practice, 34(3), 133–139. 3. Paul, M., Poyan Mehr, A., & Kreutz, R. (2006). Physiology of local renin–angiotensin systems. Physiological Re views, 86(3), 747–803. 4. Ruiz-Ortega, M., et al. (2006). Angiotensin II: A key factor in the inflammatory and fibrotic response in kidney diseases. Nephrology Dialysis Transplantation, 21(1), 16–20. 5. Sparks, M. A., et al. (2014). Classical renin–angiotensin system in kidney physiology. Comprehensive Physiology, 4(3), 1201–1228.