ANGPTL3 antibody
- Known as:
- ANGPTL3 (anti-)
- Catalog number:
- orb101655
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ANGPTL3 antibody
Related genes to: ANGPTL3 antibody
- 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: ANGPTL3 antibody
Related articles to: ANGPTL3 antibody
- Cancer remains a major global health challenge, with persistent limitations in early diagnosis, metastatic disease control, and the achievement of durable therapeutic responses with acceptable toxicity. These challenges highlight the need for more precise biomarkers and more effective therapeutic strategies. Increasing evidence implicates dysregulated lipid metabolism as a central contributor to tumor development and progression. In recent years, proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein 3 (ANGPTL3), and cholesteryl ester transfer protein (CETP) have gained particular attention due to their roles in cholesterol homeostasis, oncogenic signaling, and immune modulation within the tumor microenvironment (TME). This narrative review evaluates the potential of these lipid-regulatory mediators as diagnostic biomarkers and therapeutic targets in oncology. The majority of available evidence derives from preclinical and epidemiological studies, with PCSK9 representing the most extensively investigated target. Findings are sometimes contradictory and strongly influenced by tumor type, disease stage, and biological context, which currently precludes the clinical applicability of these molecules as reliable biomarkers. Similar limitations apply to their translational potential as actionable therapeutic targets. Nevertheless, emerging preclinical evidence suggests that modulation of these glycoproteins may enhance the efficacy of chemotherapy, targeted therapies, and immunotherapy, including nanomedicine-based approaches. Of note, clinical research investigating the role of PCSK9 inhibition in oncology is currently ongoing, whereas comparable studies focusing on ANGPTL3 and CETP remain scarce. Overall, further mechanistic, translational, and prospective clinical investigations are warranted to elucidate the involvement of these lipid-regulatory proteins in cancer biology and to define their potential integration into future oncologic diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/06/04
Kounatidis Dimitris CVallianou Natalia GPanagopoulos FotisBampiolakis AntoniosStamatopoulos VasileiosDalamaga MariaMourouzis IordanisPantos Constantinos - Residual cardiovascular risk arises from dysregulated expression of genes encoding apolipoprotein(a) (), apolipoprotein C-III (), angiopoietin-like gene 3 (), and proprotein convertase subtilisin/kexin type 9 (). RNA-based therapies, small interfering RNAs (siRNAs), and antisense oligonucleotides (ASOs) modulate these targets at the post-transcriptional level through RNA interference and RNase H-mediated degradation, respectively. This scoping review maps the molecular mechanisms, target involvement, and pharmacodynamic outcomes of RNA therapies for managing residual cardiovascular risk, with contextual comparison to traditional lipid-lowering agents. A systematic search of PubMed, Embase, Web of Science, and Scopus was performed from 2020 to February 2026. Of the 1088 records identified, 30 studies met the inclusion criteria. RNA therapies have demonstrated potential for engagement, with 80-98% reductions in Lp(a) (pelacarsen, olpasiran, zerlasiran, lepodisiran), 50-80% reductions in triglycerides (olezarsen, plozasiran, volanesorsen), and 36-44% reductions in low-density lipoprotein cholesterol (LDL-C). Mechanistically, siRNAs achieve gene silencing through RISC-mediated mRNA cleavage, with sustained pharmacodynamic effects (3-6 months) because of Argonaute-2 stability, while gapmer ASOs recruit RNase H1 for mRNA degradation. Conjugation with GalNAc allows for hepatocyte-specific delivery with a subcutaneous bioavailability of 70-85%. Safety profiles were favorable, with injection site reactions (4-12%) being the most common adverse event. This analysis maps the emerging molecular landscape of RNA therapies, highlighting their substantial precision for targeting residual cardiovascular risk pathways that cannot be addressed by traditional agents. - Source: PubMed
Publication date: 2026/05/29
Tatarciuc DianaEsanu Irina MihaelaTrandafirescu Mioara FlorentinaPauna Ana Maria RalucaVasilcu Teodor FlaviuFoia IolandaArmencia Adina OanaAntohe Magda EcaterinaGhica Dragos CatalinStamatin OvidiuVasluianu Roxana Ionela - Polycystic ovary syndrome (PCOS) is frequently accompanied by visceral obesity, insulin resistance, low-grade chronic inflammation, and metabolic syndrome (MetS). These alterations promote significant dysfunction in adipose tissue and liver metabolism through cytokine production. Growing evidence indicates that the interaction between hepatokines and adipokines plays a central role in the development of metabolic and hepatic abnormalities in women with PCOS. This narrative review was conducted to analyze the relationship between adipose tissue dysfunction and liver metabolic impairment in women with PCOS, emphasizing the involvement of hepatokines and adipokines in insulin resistance, inflammation, hepatic steatosis, hepatic fibrosis and MetS. From this perspective, contemporary clinical, biochemical, and molecular studies were reviewed to evaluate how adipocyte-derived factors and hepatocyte-derived cytokines influence metabolic homeostasis in the liver and adipose tissue in women with PCOS. Increased visceral adiposity in PCOS enhances the release of free fatty acids (FFAs) to the liver, resulting in hepatotoxicity, oxidative stress, and hepatic inflammation. Several hepatokines, including fetuin-A, angiopoietin-like protein 3 (ANGPTL3), selenoprotein P(Sep-P), and hepassocin (HPS), show abnormal circulating levels in PCOS and are strongly associated with insulin resistance, dyslipidemia, and progression to hepatic steatosis. In contrast, fibroblast growth factor 21 (FGF-21), follistatin, and interleukin (IL-6) may exert dual effects. Adipokines, such as resistin, visfatin, apelin, and retinol-binding protein 4 (RBP-4), contribute to chronic inflammation, impaired glucose metabolism, androgen excess, and hepatic steatosis and fibrosis. Some of these adipokines, such as leptin and vaspin, may exert both beneficial and detrimental effects, while others, including chemerin and omentin, appear to play predominantly beneficial roles in metabolism. Reduced adiponectin-to-leptin levels further aggravate metabolic dysfunction. These changes indicate that adipose tissue-liver crosstalk is a key mechanism linking PCOS and MetS. Overall, metabolic disturbances in PCOS are strongly mediated by dysregulated communication between adipose tissue and the liver. Altered hepatokine and adipokine profiles contribute to insulin resistance, liver dysfunction, hypertension and the development of MetS in women with PCOS. Understanding these intricate interactions may support the early identification of high-risk patients and the development of targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/06/05
de Medeiros Sebastião FreitasMaciel Gustavo Arantes Rosa - Podocyte injury constitutes the pathological basis of various glomerular diseases; however noninvasive tools for assessing podocyte injury remain limited. Angiopoietin-like protein 3 (ANGPTL3) has been shown to be pathologically elevated in glomerular diseases and is associated with podocyte injury. This study aimed to evaluate the clinical utility of the urinary ANGPTL3-to-creatinine ratio (ANGPTL3/Cre) as a noninvasive biomarker for assessing podocyte injury in children with glomerular diseases. - Source: PubMed
Publication date: 2026/06/23
Wang HengminLiu JiaojiaoDai RufengWang ChunyanChen XiaotianWang XinLiu JialuTang XiaoshanHan XinliZhai YihuiShen QianXu Hong - Polygenic scores (PGSs) stratify disease risk but often fail to capture individual variation. "Misaligned" individuals, whose observed phenotypes deviate from their genetically expected values based on PGS, provide a powerful model for identifying factors beyond common-variant effects, including additional genetic factors. Here, we apply misalignment classification and enrichment testing frameworks to seven continuous traits and three diseases, assessing whether misaligned individuals in the UK Biobank are enriched for rare (minor-allele frequency [MAF] <0.1%) damaging genetic variation. We identified significant enrichment of predicted loss-of-function (pLoF) variants in COPB2 and GORAB among individuals with lower-than-expected bone mineral density. Regarding stature, shorter-than-expected individuals were enriched for pLoF variants in ACAN and IGF1, while taller-than-expected individuals showed enrichment for damaging missense variants in FBN1. Transitioning from validation to discovery, we performed an exome-wide scan for genes associated with misalignment and identified 74 significant genes, including KANK1, a gene which may have a protective role against primary ovarian insufficiency, and ACSL6, a lipid metabolism gene where damaging missense variation was associated with lower-than-expected BMI. For diseases, results supported a liability threshold model involving counteracting common and rare variant effects. Diagnosed type 2 diabetes mellitus patients with rare pathogenic variants in HNF1A and HNF4A possessed significantly lower polygenic risk than those without. Conversely, coronary artery disease controls harboring protective ANGPTL3 variants had nominally higher polygenic risk. This study highlights the power of misalignment-based analyses in complex continuous phenotypes and disease with the potential to validate known genetic contributors to traits and identify previously unassociated genes. - Source: PubMed
Publication date: 2026/06/22
Baya Nikolas ALassen Frederik HHill BarneyVenkatesh Samvida SCurrant HannahLindgren Cecilia MPalmer Duncan S