Popa Alina Delia, Gherasim Andreea, Caba Lavinia, Niță Otilia, Graur Mariana, Mihalache Laura, Arhire Lidia Iuliana
Internal Medicine II Department, Faculty of Medicine, University of Medicine, and Pharmacy "Grigore T. Popa", 700115 Iasi, Romania.
Department of Medical Genetics, Faculty of Medicine, University of Medicine and Pharmacy "Grigore T. Popa", 16 University Street, 700115 Iasi, Romania.
Metabolites. 2024 Dec 2;14(12):672. doi: 10.3390/metabo14120672.
: 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. : 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. : 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. : 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.
LL-37与代谢综合征（MetS）相关，代谢综合征是一组包括肥胖、胰岛素抵抗（IR）、血脂异常和高血压的危险因素，会增加心血管疾病和2型糖尿病的风险。在本叙述性综述中，我们分析了聚焦于cathelicidin与代谢综合征各组成部分之间关系的最新进展的文献，以提供全面概述。研究表明，LL-37与脂肪组织（AT）中的炎症以及肥胖中IR的发展有关。Cathelicidin可通过激活促炎基因增强炎症反应，并调节炎症反应。IR的机制包括激活诱导炎症并降低脂肪细胞中胰岛素信号传导的复杂信号通路。Cathelicidin激活Toll样受体（TLRs）会刺激促炎细胞因子的分泌，导致脂肪细胞中胰岛素功能的破坏。Cathelicidin还影响脂质代谢，最近的研究表明LL-37水平与高密度脂蛋白胆固醇之间呈负相关。因此，LL-37不仅参与炎症调节，还参与脂质代谢，可能会加重与代谢综合征相关的心血管并发症。Cathelicidin在调节代谢综合征中炎症和抗炎反应之间的平衡方面起着关键作用。了解LL-37对这些机制的影响可能会揭示解决代谢综合征及其相关并发症的新方法。
