: 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.
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http://dx.doi.org/10.3390/metabo14120672 | DOI Listing |
Curr Pharm Des
January 2025
Center for Global Health Research, Saveetha Medical College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.
Background: In vascular tissue, macrophages and inflammatory cells produce the enzyme lipoprotein- associated phospholipase A2 (Lp-PLA2). Treatment with fibrates decreases Lp-PLA2 levels in individuals with obesity and metabolic syndrome; however, these findings have not been fully clarified.
Objective: The goal of this study was to investigate the possible effects of fibrate therapy on Lp-PLA2 mass and activity through a meta-analysis of clinical trials.
Bioessays
January 2025
Centre for Regenerative Medicine, Institute of Regeneration and Repair, The University of Edinburgh, Edinburgh, Scotland, UK.
Case Rep Dent
January 2025
Faculty of Dental Sciences, Beirut Arab University, Beirut, Lebanon.
Mucopolysaccharidosis (MPS) Type III (MPS III) or Sanfilippo syndrome is a rare autosomal recessive inherited metabolic disorder. This disorder is responsible for lysosomal storage disorder at the cellular aspect. Due to lysosomal enzyme perturbance leading to the alteration of macromolecule metabolisms, this cellular perturbance causes multiple severe systemic and mental outcomes.
View Article and Find Full Text PDFHeliyon
January 2025
Sinopharm Dongfeng General Hospital, Hubei Clinical Research Center of Hypertension, Hubei University of Medicine, Shiyan, 442008, China.
Apigenin is a natural flavonoid abundantly found in fruits, vegetables, and medicinal plants. It possesses protective effects against cancer, metabolic syndrome, dyslipidemia, etc. Atherosclerosis, a chronic immune-mediated inflammatory disease, is the underlying cause of coronary heart disease, stroke, and myocardial infarction.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of Dermatology, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, People's Republic of China.
Purpose: Psoriasis is a complex inflammatory skin disorder that is closely associated with metabolic syndrome (MetS). Limited information is available on skin metabolic changes in psoriasis; the effect of concurrent MetS on psoriatic skin metabolite levels is unknown. We aimed to expand this information through skin metabolomic analysis.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!