Eurasian Journal of Medical and Natural Sciences 6-jild 8-son (2026) · 11–23-betlar

METABOLIK SINDROMDA IMMUN YALLIG'LANISHNING PATOGENETIK AHAMIYATI VA ZAMONAVIY DAVOLASH USULLARI (Adabiyotlar sharhi)

Kazaxbayeva, Gulistan

DOI: 10.5281/zenodo.21913349 · Manbada o'qish → · PDF (manba serverida)

Annotatsiya

Metabolic syndrome (MS) is a complex pathophysiological condition that combines central obesity, insulin resistance, atherogenic dyslipidemia, and arterial hypertension, affecting a significant portion of the global population and serving as a primary risk factor for developing type 2 diabetes and cardiovascular diseases. Research conducted in recent years consistently confirms that chronic low-grade "sterile" inflammation—metaphylaxis (metabolic inflammation) —is the fundamental link in the pathogenesis of MS. This process is carried out through a chain of closely related pathogenetic links, such as fatty tissue dysfunction, shifting macrophage polarization to the pro-inflammatory M1 phenotype, activation of the NLRP3 inflammasome system, Treg/Th17 imbalance, and intestinal microbiota dysbiosis. This literature review highlights the immune-inflammatory pathogenesis of MS from a modern perspective and analyzes innovative therapeutic approaches aimed at these mechanisms - lifestyle modification, metformin, statins, GLP-1 receptor agonists, SGLT2 inhibitors, targeted biological drugs targeting cytokines, and bariatric surgery. The obtained conclusions are of great scientific and practical importance for practicing clinicians in forming a pathogenetically sound, individualized, and multidisciplinary treatment strategy for metabolic syndrome.

Metabolic syndrome; chronic inflammation; metainflammation; insulin resistance; NLRP3-inflammasoma; adipokines; macrophage polarization; intestinal microbiota; GLP-1 receptor agonists; SGLT2 inhibitors.Metabolik sindrom; surunkali yallig'lanish; metaflammatsiya; insulinorezistentlik; NLRP3-inflammasoma; adipokinlar; makrofag polarizatsiyasi; ichak mikrobiotasi; GLP-1 retseptor agonistlari; SGLT2 ingibitorlari.

Metadata manbasi: jurnal OAI-PMH arxivi · Sindex to'liq matnni saqlamaydi, manbaga havola beradi.