Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Amyloid-beta (Aβ) is a key factor in the onset and progression of Alzheimer's disease (AD). Selenium (Se) compounds show promise in AD treatment. Here, we revealed that selenoprotein K (SELENOK), a selenoprotein involved in immune regulation and potentially related to AD pathology, plays a critical role in microglial immune response, migration, and phagocytosis. In vivo and in vitro studies corroborated that SELENOK deficiency inhibits microglial Aβ phagocytosis, exacerbating cognitive deficits in 5xFAD mice, which are reversed by SELENOK overexpression. Mechanistically, SELENOK is involved in CD36 palmitoylation through DHHC6, regulating CD36 localization to microglial plasma membranes and thus impacting Aβ phagocytosis. CD36 palmitoylation was reduced in the brains of patients and mice with AD. Se supplementation promoted SELENOK expression and CD36 palmitoylation, enhancing microglial Aβ phagocytosis and mitigating AD progression. We have identified the regulatory mechanisms from Se-dependent selenoproteins to Aβ pathology, providing novel insights into potential therapeutic strategies involving Se and selenoproteins.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10850786 | PMC |
| http://dx.doi.org/10.1016/j.redox.2024.103064 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Microfluidic Generation of Oxidized Phospholipid Gradients in Supported Lipid Bilayers to Examine Scavenger Receptor Interactions.
Anal Chem
September 2025
Department of Chemistry, Lehigh University, 6 East Packer Avenue, Bethlehem, Pennsylvania 18015, United States.
Reactive oxygen species (ROS) are responsible for the oxidative truncation of polyunsaturated fatty acids (PUFAs). The products of these reactions have been implicated in many diseases such as cancer and atherosclerosis. As increasing attention is directed toward these oxidized phospholipids (oxPLs), higher throughput methods are needed to examine interactions between oxPLs and scavenger receptors in the immune system.
View Article and Find Full Text PDFLipid overload meets S-palmitoylation: a metabolic signalling nexus driving cardiovascular and heart disease.
Cell Commun Signal
September 2025
Cardiovascular Department, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, 42 Wenhuaxi Road, Jinan, Shandong, China.
S-palmitoylation has emerged as a critical integrator of lipid overload and cardiovascular dysfunction. Disordered lipid metabolism inundates endothelial cells, vascular smooth muscle cells and macrophages with triglyceriderich lipoproteins, oxidized LDL and saturated fatty acids, expanding the intracellular palmitoylCoA pool and perturbing redox balance. Protein Spalmitoylation, the reversible attachment of palmitate to cysteine residues, converts excess palmitoylCoA into broad alterations in signalling and membrane dynamics.
View Article and Find Full Text PDFPalmitoylation-dependent modulation of CD36 trafficking and signaling integrates lipid uptake with metabolic disease pathogenesis.
Pharmacol Res
August 2025
Key Laboratory of Animal Genetics & Breeding and Molecular Design of Jiangsu province, College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China. Electronic address:
CD36 is a multifunctional lipid transporter that facilitates long-chain fatty acid uptake and orchestrates metabolic signaling in energy-demanding tissues. Recent studies have uncovered site-specific palmitoylation as a crucial post-translational modification that governs CD36 subcellular trafficking, stabilizing its localization within lipid rafts and regulating its endocytic recycling between the plasma membrane, endosomes, and lipid droplets. This dynamic palmitoylation-depalmitoylation cycle enables CD36 to spatially and temporally couple lipid transport with signal transduction in response to nutritional and hormonal cues.
View Article and Find Full Text PDFExtracellular Vesicles From Limosilactobacillus johnsonii Enhance Milk Fat Synthesis by Inducing CD36 Dynamic Palmitoylation and Activating PPARγ Signalling.
J Extracell Vesicles
August 2025
Guangdong Province Key Laboratory of Animal Nutrition Control, College of Animal Science, South China Agricultural University, Guangzhou, China.
Mammals support offspring survival through efficient milk production, ensuring the transfer of essential nutrients and energy. Extracellular vesicles (EVs) released by gut microorganisms function as signalling molecules that influence host physiology. In this study, we observed an association between gut microbiota and lactation performance, with Limosilactobacillus johnsonii showing potential in promoting milk fat synthesis.
View Article and Find Full Text PDFInhibiting CD36 palmitoylation improves cardiac function post-infarction by regulating lipid metabolic homeostasis and autophagy.
Nat Commun
July 2025
State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), College of Pharmacy, and Department of Cardiology, the Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Alterations in myocardial energy substrate metabolism and mitochondrial injury following myocardial infarction (MI) lead to structural and functional abnormalities of the heart. The fatty acid translocase CD36 (CD36) plays a pivotal role in regulating lipid homeostasis and mitochondrial metabolism. Here, we demonstrate that inhibiting the palmitoylation of CD36 and the resulting alteration in its subcellular localization alleviates lipid metabolism disorders and mitochondrial dysfunction in cardiomyocytes of male mice post-MI.
View Article and Find Full Text PDF