Crosstalk between inflammasomes, inflammation, and Nrf2: Implications for gestational diabetes mellitus pathogenesis and therapeutics

Abstract

The role of inflammasomes in gestational diabetes mellitus (GDM) has emerged as a critical area of research in recent years. Inflammasomes, key components of the innate immune system, are now recognized for their involvement in the pathogenesis of GDM. Activation of inflammasomes in response to various triggers during pregnancy can produce pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and interleukin-18 (IL-18), contributing to systemic inflammation and insulin resistance. This dysregulation not only impacts maternal health but also poses significant risks to fetal development and long-term health outcomes. Understanding the intricate interplay between inflammasomes and GDM holds promise for developing novel therapeutic strategies and interventions to mitigate the adverse effects of this condition on both mothers and their offspring. Researchers have elucidated that targeting inflammasomes using anti-inflammatory drugs and compounds can effectively reduce inflammation in GDM. Furthermore, the addition of nuclear factor erythroid 2-related factor 2 (Nrf2) to this complex mechanism opens novel avenues for therapeutics. The antioxidant properties of Nrf2 may potentially suppress inflammasome activation in GDM. This comprehensive review investigates the intricate relationship between inflammasomes and GDM, emphasizing the pivotal role of inflammation in its pathogenesis. It also sheds light on potential therapeutic strategies targeting inflammasome activation and explores the role of Nrf2 in mitigating inflammation in GDM.

Keywords: Diabetes mellitus; GDM; Inflammasomes; NLRP3; Nrf2.