Cathelicidin: Insights into Its Impact on Metabolic Syndrome and Chronic Inflammation

Abstract

Background/Objectives: LL-37 is associated with metabolic syndrome (MetS), a constellation of risk factors comprising obesity, insulin resistance (IR), dyslipidemia, and hypertension, which elevates the risk of cardiovascular disease and type 2 diabetes. Methods: In this narrative review, we analyzed the literature focusing on recent developments in the relationship between cathelicidin and various components of MetS to provide a comprehensive overview. Results: Studies have shown that LL-37 is linked to inflammation in adipose tissue (AT) and the development of IR in obesity. Cathelicidin can enhance inflammation by activating pro-inflammatory genes, as well as modulate the inflammatory response. The mechanisms of IR include the activation of complex signaling pathways that induce inflammation and reduce insulin signaling in adipocytes. The activation of Toll-like receptors (TLRs) by cathelicidin stimulates the secretion of pro-inflammatory cytokines, contributing to the disruption of insulin function in adipose cells. Cathelicidin also influences lipid metabolism, with recent research showing a negative relationship between LL-37 levels and HDL cholesterol. Therefore, LL-37 is involved not only in the regulation of inflammation but also in lipid metabolism, potentially aggravating the cardiovascular complications associated with MetS. Conclusions: Cathelicidin plays a crucial role in regulating the balance between inflammatory and anti-inflammatory responses in MetS. Understanding the impact of LL-37 on these mechanisms may unveil novel approaches for addressing MetS and its associated complications.