APOC3 ELISA kit
- Known as:
- APOC3 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APOC3-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APOC3 ELISA kit
Related genes to: APOC3 ELISA kit
- Gene:
- APOC3 NIH gene
- Name:
- apolipoprotein C3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-04-26
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- Lipid accumulation drives the development of atherosclerotic cardiovascular disease, the leading cause of death worldwide. The liver is the primary target for lipid-lowering therapies due to its central role in lipid metabolism. Despite advances in small-molecule drugs, substantial residual cardiovascular risk remains. Recent clinical evidence in 2026 reaffirms the "lower is better" paradigm, showing that achieving very low low-density lipoprotein cholesterol (<55 mg/dl) improves outcomes versus standard goals (<70 mg/dl). RNA-targeted therapeutics, including antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs), offer a transformative approach by durably silencing genetically validated lipid targets. Conjugation to -acetylgalactosamine (GalNAc) enables hepatocyte-specific delivery. Examples include inclisiran (targeting proprotein convertase subtilisin/kexin type 9 [PCSK9]) and agents against apolipoprotein C-III (APOC3), lipoprotein(a) [Lp(a)], and angiopoietin-like protein 3 (ANGPTL3). Beyond protein-coding messenger RNAs (mRNAs), RNA therapeutics can also target noncoding RNAs (microRNAs and long noncoding RNAs) that regulate cholesterol homeostasis. Additionally, mRNA lipid nanoparticle-based in vivo base editing (e.g., VERVE 101/102 targeting PCSK9) has entered clinical trials, offering potential for permanent genetic correction with a single infusion. In the future, RNA-targeted therapeutics may expand beyond hepatic lipid modulation to directly target vascular lipid metabolism and plaque biology. Advances in extrahepatic delivery and rational combination regimens could transform RNA therapy from transient lipid-lowering to long-term, disease-modifying interventions. The recent 2026 American College of Cardiology/American Heart Association dyslipidemia guideline emphasizes the clinical importance of targeting PCSK9, APOC3, Lp(a), and ANGPTL3. This review provides a state-of-the-art overview of RNA-targeted therapeutics in hyperlipidemia and discusses future research directions in this emerging field. - Source: PubMed
Publication date: 2026/05/19
Ali IqraQiu JuhuiCheang Wai SanWang GuixueXu Suowen - Despite effective control of low-density lipoprotein cholesterol, the residual risk of atherosclerotic cardiovascular disease (ASCVD) remains substantial, underscoring the urgent need to identify novel targets to further reduce ASCVD risk. This study aimed to investigate the association between apolipoprotein C-III (APOC3) levels and ASCVD, and further explore the potential impact of APOC3 intervention for reducing ASCVD risk. - Source: PubMed
Deng XuanLiu YanJia Ping-PingZhang Yu-HanDeng Qiu-JvHao Yong-ChenYang NaHan Li-ZhenSun Jia-YiLu Wen-TingSun Xue-TingQi YueYang ZhaoLiu Jing - Reducing plasma levels of low-density lipoprotein cholesterol (LDL-C) is the cornerstone in the prevention of coronary artery disease (CAD) but may also increase risk of type 2 diabetes (T2D). A comprehensive examination of the genetic evidence of T2D related side-effects of all current lipid-modifying drugs, including those in development, has not yet been performed. - Source: PubMed
Publication date: 2026/05/14
Chen ZekaiTriatin Rima DLuo LiSnieder HaroldSchmidt A FloriaanDitmarsch MarcKastelein John J PDullaart Robin P FKuivenhoven Jan AlbertThio Chris H L - Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating condition associated with approximately 30% mortality and 20% severe disability among survivors. Delayed cerebral ischemia due to cerebral vasospasm and hydrocephalus significantly contribute to poor neurological outcomes. Currently, reliable biomarkers for early prediction of these complications remain lacking. In this study, 63 patients with a mean age of 59.7 ± 11.53 years were enrolled. Functional outcomes were assessed by the modified Rankin Scale (mRS). Cerebrospinal fluid (CSF) samples were obtained through lumbar drainage (LD) or external ventricular drainage (EVD) and analyzed by ELISA. The predictive value of biomarkers was evaluated using receiver operating characteristic (ROC) curve analysis. Elevated Apolipoprotein C-III (ApoC3) levels in CSF of aSAH patients were observed. Furthermore, increased ApoC3 concentrations were significantly associated with poor prognosis and an elevated risk of severe complications. At an optimal cutoff value of 4,463 ng/mL, patients with high ApoC3 levels exhibited significantly worse 3-month functional outcomes and a higher incidence of delayed cerebral ischemia and hydrocephalus. Monitoring ApoC3 levels in CSF may be beneficial for predicting complications such as delayed cerebral ischemia and hydrocephalus in patients with aSAH. - Source: PubMed
Publication date: 2026/04/17
Tong BinWang JunjieChen JiaruiZhang QiaXu ZhouhanYang KaichuangChen Xiaomin - Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by hepatic triglyceride accumulation in the setting of obesity and insulin resistance. Although apolipoprotein C-III (APOC3) is a well-established regulator of plasma triglyceride metabolism, its hepatocyte-intrinsic role in intracellular lipid accumulation remains unclear. In this study, we investigated whether APOC3 contributes to hepatocellular triglyceride synthesis during early metabolic dysfunction. In 6-week-old db/db mice, early hepatic lipid accumulation was observed without detectable fibrosis. Transcriptomic profiling identified as an upregulated gene associated with lipid metabolic pathways, and its hepatic upregulation was confirmed at both mRNA and protein levels. Gain- and loss-of-function experiments in HepG2 cells demonstrated that APOC3 overexpression significantly increased intracellular triglyceride content, whereas APOC3 knockdown reduced triglyceride accumulation. Mechanistically, APOC3 selectively regulated diacylglycerol acyltransferase 2 (DGAT2), which catalyzes the final step of triglyceride synthesis, without significantly affecting major lipogenic transcription factors. Furthermore, under de novo lipogenesis-inducing conditions triggered by the liver X receptor agonist T0901317 and insulin, APOC3 markedly amplified DGAT2 expression and triglyceride accumulation. Collectively, these findings suggest a hepatocyte-intrinsic role for APOC3 in promoting triglyceride accumulation through DGAT2-dependent mechanisms. The APOC3-DGAT2 axis may represent a relevant pathway contributing to hepatic lipid accumulation in metabolic liver disease. - Source: PubMed
Publication date: 2026/04/20
Nguyen Thi NhiKim Hye-JeongShim Hye MinKang JunhoHa Eun YoungCho HochanPark Jae-Hyung