ApoB antibody
- Known as:
- ApoB (anti-)
- Catalog number:
- 10-1840
- Product Quantity:
- 200 ul
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- ApoB antibody
Related genes to: ApoB antibody
- Gene:
- APOB NIH gene
- Name:
- apolipoprotein B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: ApoB antibody
Related articles to: ApoB antibody
- Lipoprotein(a) [Lp(a)] is a genetically determined, independent risk factor for atherosclerotic cardiovascular disease and calcific aortic valve stenosis. Plasma Lp(a) levels are 70-90% heritable, largely unresponsive to lifestyle changes, and poorly controlled with typical lipid-lowering drugs such as statins and PCSK9 inhibitors. The development of powerful RNA-based therapies offers a new chance to specifically target and significantly lower Lp(a). We examined available phase 1-3 trial data, regulatory updates, and trial registries up to mid-2026 to provide an overview of the current pipeline, ongoing cardiovascular outcomes trials (CVOTs), and new mechanistic and genomic methods. - Source: PubMed
Publication date: 2026/08/13
Ebubechukwu UgochukwuUgoala OnyinyeShahid RameenKulkarni Anandita - Knee osteoarthritis (KOA) is a heterogeneous whole-joint disorder in which mechanical loading, aging, metabolic stress, synovitis, microvascular dysfunction, matrix injury, subchondral remodeling, pain-related neurovascular change, and impaired repair interact over time. The infrapatellar fat pad (IFP) is increasingly recognized as an active synovio-adipose tissue, yet IFP inflammation, lipid disturbance, hypoxia, angiogenesis, matrix catabolism, and subchondral change are often considered parallel abnormalities rather than as a spatially organized propagation process. This Perspective proposes an IFP-centered spatial lipid-barrier coupling framework for a biologically enriched KOA subset. The central claim is not that lipid quantity alone drives KOA, but that lipid-derived signals become mechanistically meaningful when they appear in vulnerable barrier-defined spaces and co-localize with permeability injury, hypoxia, inflammatory execution, oxidative-matrix injury, or impaired repair. In this model, lipid-spatial mislocalization is a candidate threshold event, lipid-cytokine-hypoxia-barrier coupling is the progression engine, and barrier-defined propagation links the IFP, synovium, synovial cavity, cartilage matrix, osteochondral interface, and subchondral marrow-adipose compartment. Current evidence supports active IFP biology, IFP-synovium communication, circulation-to-joint-fluid access, multi-compartment lipid disturbance, HIF/VEGF and FFA-NOX/ROS pathways, and subchondral marrow involvement. However, source-resolved spatial co-localization and temporal ordering remain unproven. The framework should therefore be retained only if a reproducible lipid-barrier signature predicts progression, pain biology, or treatment response beyond synovitis, body mass index, malalignment, bone marrow lesions, and radiographic severity. - Source: PubMed
Publication date: 2026/08/11
Liu YuwuChen MingYong Ruhua - This study integrated an in vivo feeding trial (0.00-1.00% choline chloride) with in vitro primary hepatocyte experiments to elucidate the molecular mechanisms by which choline chloride alleviates hepatic lipid deposition in bighead carp. The results showed that dietary supplementation with 0.80-1.00% choline chloride significantly reduced hepatic triglyceride (TG) content and lipid droplet accumulation. At the molecular level, choline markedly downregulated lipogenic genes (, , ) while upregulating genes involved in lipolysis (, ) and lipid transport (, ). Non-targeted lipidomics revealed that choline maintains lipid homeostasis primarily via the glycerophospholipid metabolism pathway, significantly increasing levels of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS). Furthermore, choline intervention enhanced the expression of its own metabolism-related genes (, , , ), accelerating choline transport and phosphorylation. Overall, based on the results of this experiment, 0.80% is the recommended supplemental level of choline chloride in diets, which can effectively alleviate lipid deposition in bighead carp. The mechanism involves inhibiting lipogenesis and promoting lipid decomposition and transport through glycerophospholipid pathways, while simultaneously enhancing PC synthesis to accelerate hepatic lipid export. These findings provide a theoretical basis for precise feed formulation in bighead carp. - Source: PubMed
Publication date: 2026/08/01
Sun HuiminChen JunWang ChengjieHuang FengZhuo Meiqin - Primary hyperlipoproteinemias represent a heterogeneous group of inherited lipid metabolism disorders characterized by persistent abnormalities in plasma lipoproteins, a markedly increased risk of premature atherosclerotic cardiovascular disease (ASCVD) and, in selected phenotypes, acute pancreatitis. Traditionally classified according to the Fredrickson phenotypic system, these disorders are now increasingly understood through a multidimensional framework integrating molecular genetics, intracellular lipid trafficking, inflammatory signaling, and systemic metabolic regulation. Recent advances have identified both monogenic and polygenic determinants underlying disease expression, including pathogenic variants affecting LDLR, APOB, PCSK9, APOE, and lipoprotein lipase pathways, as well as the cumulative contribution of multiple common lipid-associated variants. Furthermore, emerging evidence highlights the role of endoplasmic reticulum stress, oxidative imbalance, adipose-hepatic crosstalk, intestinal lipid absorption, and inflammatory mediators in modulating lipoprotein metabolism and cardiovascular risk. Novel regulators such as angiopoietin-like proteins (ANGPTLs), microRNAs, and pathways involved in cholesterol efflux and remnant lipoprotein clearance have further refined our understanding of disease heterogeneity and therapeutic responsiveness. Familial hypercholesterolemia and familial combined hyperlipidemia exemplify the complex interplay between genetic susceptibility, metabolic dysfunction, and environmental influences that shape phenotype severity and long-term cardiovascular outcomes. Advances in diagnostic strategies, including genetic testing, polygenic risk scores, apolipoprotein profiling, and vascular imaging, have significantly improved risk stratification and personalized management. Simultaneously, innovative therapies-including PCSK9 inhibitors, ANGPTL3-targeted agents, antisense oligonucleotides, and RNA-silencing technologies-are reshaping treatment paradigms and expanding options for high-risk patients. This chapter synthesizes contemporary insights into the pathogenesis of primary hyperlipoproteinemias, emphasizing the transition from traditional lipid-based classification toward precision medicine approaches focused on lifetime cardiovascular risk, molecular characterization, and individualized therapeutic intervention. - Source: PubMed
Publication date: 2026/07/23
Bararu-Bojan IrisVladeanu Maria CristinaIliescu-Halitchi DanPlesoianu Carmen ElenaBojan AndreiFrasinariu Otilia ElenaTudor Razvan CosminCiocoiu ManuelaTudor CatalinaIliescu-Hailitchi CodrutaBazyani AminFoia Cezar IlieBadulescu Oana-Viola - Eggs serve as an indispensable global nutritional resource, sustaining the economic foundation of the commercial poultry industry. To meet this continuous demand, egg formation involves an exceptionally energy-intensive biological process requiring continuous yolk precursor synthesis, which imposes a massive metabolic burden on laying hens. However, the comprehensive metabolic differences across the gut-liver-adipose axis between peak laying hens with high or low egg production remain incompletely characterized. A total of 180 healthy Hy-Line Brown laying hens (45-week-old) were continuously fed and monitored for production performance over a 6-week period. Following the exclusion of individuals with extremely low egg production (≤10 eggs during the 6-week monitoring period; n = 5) and candidate hens that repeatedly produced unqualified eggs over multiple weeks (n = 20), the remaining hens were ranked by 6-week average laying rate and allocated into FH (high-production hens at 50 weeks of age, n = 15) and FL (low-production hens at 50 weeks of age, n = 14) groups. Initial body weight did not differ significantly between groups (FH: 1936 ± 29.0 g; FL: 1894 ± 48.2 g; P-value = 0.446). We integrated transcriptomic, untargeted metabolomic, targeted bile acid metabolomics, and microbiome (16S rRNA and metagenomic) profiles to characterize comprehensive metabolic changes across the gut-liver-adipose axis associated with divergent egg-production phenotypes. The results showed that: (1) FH hens exhibited higher serum APOB and lower conjugated bile acids (TCDCA, TCA, and THDCA), with hepatic upregulation of FASN, PPARA, CPT1A, and VTG1 along with downregulation of CYP7A1, CYP7B1, CYP8B1, and CYP27A1; (2) intersecting module hub genes (MHGs) with differentially expressed genes (DEGs) identified 354 upregulated and 299 downregulated core genes, with EEF2 identified as the primary hepatic downregulated hub gene; (3) in abdominal fat, GSEA revealed significant enrichment in fatty acid transport (NES = 1.54), long-chain fatty acid metabolic process (NES = 1.39), and steroid hormone biosynthesis (NES = 1.85), accompanied by significant downregulation of ANGPTL4 and upregulation of HSD3B1, VTG1, VTG2, and VTG3; (4) ileal mucosal transcriptomics identified 619 DEGs (502 upregulated), with GSEA highlighting enrichment in cell junction organization (NES = 1.52) and tube morphogenesis (NES = 1.39), which were further categorized into functional modules including enteric synaptic signaling, epithelial adhesion, mucosal vascularization, and tissue renewal; (5) the functional profile of the ileal microbiota in FH hens showed enrichment of functions related to complex carbohydrate degradation and carbohydrate-binding modules, with keystone taxa including Blautia and Bifidobacterium associated with production and lipid markers. Collectively, these findings suggest that high egg production during the peak laying period is associated with coordinated metabolic differences across the liver, abdominal fat tissue, and intestine. The observed profiles included reduced hepatic translation-related and primary bile acid synthesis-related signatures, adipose endocrine-related changes and microbial functional potential related to carbohydrate utilization and antioxidant-related functional potential. These findings provide candidate multi-omics features for precision nutritional strategies and genetic improvement in commercial poultry. - Source: PubMed
Publication date: 2026/07/27
Ma JunjieQin KailongQiao ZhihaoRen ZhouzhengYang XiaojunLiu Yanli