IMMUNOMODULATORY AND ANTI-INFLAMMATORY EFFECTS OF SGLT2 INHIBITORS IN CARDIOVASCULAR PATHOLOGY

Abstract

Cardiovascular diseases (CVDs) have long remained the leading cause of disability and mortality worldwide. The modern concept of cardiology views chronic low-grade systemic inflammation as a fundamental pathogenic mechanism that triggers and accelerates atherosclerosis, myocardial remodeling, and fibrosis [3, 4]. Consequently, the search for drugs possessing synergistic metabolic and anti-inflammatory properties represents a strategic imperative. The discovery of pronounced extra-pancreatic effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors has radically transformed therapeutic approaches to heart failure and ischemic heart disease [5]. This class of drugs (dapagliflozin, empagliflozin, etc.) not only optimizes hemodynamics and energy metabolism but also exhibits powerful immunomodulatory potential. Specifically, SGLT2 inhibitors are capable of regulating the phenotypic polarization of macrophages, suppressing the activity of the pro-inflammatory M1 pool and activating the protective anti-inflammatory M2 pool. This results in a reduction in serum levels of key cytokines (interleukins 1\(\beta \) and 6, tumor necrosis factor-alpha) and mitigates inflammatory infiltration in cardiac and vascular tissues. A profound study and systematization of the molecular and cellular mechanisms underlying this anti-inflammatory action are essential for expanding the indications for SGLT2 inhibitors and developing targeted programs for personalized cardioprotection.