Human Angiopoietin-like 3 / ANGPTL3 Protein
- Known as:
- Human Angiopoietin-like 3 / ANGPTL3 Protein
- Catalog number:
- AN3-H5226
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human Angiopoietin-like 3 / ANGPTL3 Protein
Related genes to: Human Angiopoietin-like 3 / ANGPTL3 Protein
- Gene:
- ANGPTL3 NIH gene
- Name:
- angiopoietin like 3
- Previous symbol:
- ANGPT5
- Synonyms:
- -
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-07
- Date modifiied:
- 2015-11-11
Related products to: Human Angiopoietin-like 3 / ANGPTL3 Protein
Related articles to: Human Angiopoietin-like 3 / ANGPTL3 Protein
- CRISPR-based base editors hold transformative potential for genetic medicine, but their clinical translation is hampered by the need for cell-specific delivery, efficient cytosolic release, and durable activity. Here, we report a dual-functional poly(disulfide) that simultaneously achieves both hepatocyte-specific targeting and direct cytosolic delivery of adenine base editors (ABEs). By displaying galactose ligands for binding to asialoglycoprotein receptors (ASGPRs) on hepatocytes, our polymer enables specific recognition of hepatocytes. Crucially, the poly(disulfide) backbone then facilitates direct cytosolic delivery via thiol-disulfide exchange, bypassing endosomal entrapment. This dual-function system mediates efficient ABEs delivery to hepatocytes, resulting in durable editing of the ANGPTL-3 gene after a single administration. In a mouse model of atherosclerosis, this one-dose treatment produced sustained reductions in low-density lipoprotein cholesterol and significantly attenuated plaque formation. To our knowledge, this represents the first successful application of base editing for the effective prevention and treatment of atherosclerosis with a single-dose. Our work establishes a "once-and-for-all" atherosclerosis treatment that creates a transformative platform for precision genome medicine in atherosclerosis and other metabolic diseases. - Source: PubMed
Publication date: 2026/05/23
Zhang XiaopingGao ShijuanChen DanyangWang HongyingZuo MinzanWang LeyongZhang Qing-WenWang Ruibing - Hepatic steatosis, the hallmark of metabolic dysfunction-associated steatotic liver disease (MASLD), is closely associated with elevated plasma and intrahepatic triglyceride (TG) levels, often driven by insulin resistance, atherogenic dyslipidemia, and metabolic syndrome. Growing evidence suggests that triglyceride-lowering therapies may not only improve systemic lipid profiles but also directly impact hepatic fat accumulation and associated inflammation and fibrosis. This review explores current and emerging TG-lowering therapies, including fibrates, omega-3 fatty acids, pemafibrate, and novel agents such as pegozafermin (an FGF21 analog), and APOC3 and angiopoietin-like protein 3 (ANGPTL3) inhibitors, in the context of hepatic steatosis and MASLD. We discuss the mechanistic rationale behind TG-lowering as a therapeutic strategy, summarize key preclinical and clinical trial findings, and evaluate their effects on liver fat content, liver enzymes, fibrosis markers, and histologic outcomes. While several agents demonstrate promise in reducing intrahepatic fat deposition and improving liver-related outcomes, further large-scale studies are required to establish their long-term efficacy and safety, and potential for disease modification in MASLD/metabolic dysfunction-associated steatohepatitis (MASH). Triglyceride-targeted therapies may offer a valuable adjunct or complementary approach to current treatment paradigms focused on weight loss, insulin sensitization, and antagonizing inflammation. - Source: PubMed
Publication date: 2026/05/12
Tamehri Zadeh Seyed SaeedToth Peter PBanach Maciej - In this paper, we review the literature regarding metformin's action on blood lipid concentrations in metformin-treated diabetic patients. Published data indicate that metformin reduces serum total cholesterol (T-C), LDL-cholesterol (LDL-C) and triacylglycerol (TAG) concentrations and raises serum HDL-cholesterol (HDL-C) concentrations in diabetic patients. The beneficial effect of metformin on serum lipid profiles in diabetic patients can result from (a) its action on AMP-activated protein kinase, which inhibits lipogenesis and cholesterol synthesis and stimulates fatty acid oxidation; (b) decreased plasma TAG concentrations, via promoting VLDL-TAG clearance by brown adipose tissue; (c) the inhibition of nuclear factor erythroid 2-related factor 2 () gene expression, affecting lipid profile in diabetic patients; (d) the inhibition of the expression of genes encoding proprotein convertase subtilisin/kexin 9 (PCSK9) and lipogenic enzymes; (e) the downregulation of carbohydrate-response element-binding protein (ChREBP), which affects liver TAG and cholesterol synthesis from acetate formed by gut microbiota; (f) the inhibition of angiopoietin-like 3 protein (ANGPTL3) gene expression, and consequent effects on plasma TAG concentrations; (g) the activation of AMPK, which inhibits LXRα activity; and (h) reverse cholesterol transport. In conclusion, one can assume that beyond its primary antihyperglycemic effect, metformin exerts pleiotropic effects that modulate lipid metabolism and blood lipid profile in T2D patients. These beneficial effects of metformin on blood lipid profile may play a role in the reduction in cardiovascular risk in diabetic patients. - Source: PubMed
Publication date: 2026/05/21
Dettlaff-Pokora AgnieszkaSwierczynski Julian - 1. Lipids are fundamental regulators of cellular structure, energy balance, and signalling, while their dysregulation contributes significantly to the development of chronic diseases. 2. Recent advances in multi-omics technologies, including genomics, transcriptomics, proteomics, metabolomics, lipidomics, and epigenomics, have transformed the investigation of lipid metabolism by enabling high-resolution characterisation of lipid species, metabolic pathways, and regulatory networks. 3. This review emphasises the significance of lipids in chronic metabolic diseases like cardiovascular disease, type 2 diabetes mellitus, metabolic syndrome, non-alcoholic fatty liver disease, neurodegenerative disorders, cancer, and chronic kidney disease. 4. The discovery of various biomarkers of disease conditions lipidomics analysis includes lipids such as ceramides, oxidised phospholipids, acylcarnitines, and lysophospholipids, which have been implicated in causing inflammation, oxidative stress, mitochondrial dysfunction, and fibrosis. 5. Omics integration can aid in obtaining new perspectives in understanding disease pathophysiology and help in identifying novel therapeutic targets including PCSK9 (Proprotein convertase subtilisin/kexin type 9), ANGPTL3 (Angiopoietin-like 3), and inflammatory lipids. Recent lipidomics platforms like spatial lipidomics and single-cell lipidomics may add value in developing personalised medicine therapies. - Source: PubMed
Publication date: 2026/05/31
Majumder DebashritaBhattacharya DebasmitaSingh Gill HarjotRajeev MithulSharma ShubhamDwivedi Shashi PrakashNag MoupriyaLahiri Dibyajit - Remnant cholesterol (RC), the cholesterol transported in triglyceride-rich lipoprotein (TRL) remnants, has emerged as a major contributor to residual atherosclerotic cardiovascular disease (ASCVD) risk. We review epidemiologic, genetic, and interventional data supporting TRL-remnant cholesterol (TRL-RC) as a causal risk factor and outline concrete implications for cardiovascular outcomes trial design. - Source: PubMed
Publication date: 2026/05/24
Rosenson Robert SVelamuri Deepthi NishiMuntner PaulGoonewardena Sascha N