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
- Individuals with type 1 diabetes (T1D) have increased mortality from cardiovascular disease (CVD) compared to general population, where hypertension is a major risk factor. The aim of this study was to evaluate blood pressure (BP) and arterial stiffness in young adults with childhood-onset T1D compared to healthy control subjects. - Source: PubMed
Publication date: 2026/05/15
Simeunovic AidaBrunborg CathrineHeier MartinBerg Tore JulsrudDahl-Jørgensen KnutMargeirsdottir Hanna Dis - Coronary microvascular dysfunction (CMD) has emerged as a crucial contributor to cardiovascular morbidity and mortality, particularly in patients with ischemia and non-obstructive coronary arteries (INOCA). The condition arises from a complex interplay of structural and functional abnormalities within the small coronary vessels, driven by underlying molecular mechanisms including endothelial nitric oxide synthase (eNOS) uncoupling, oxidative stress, and chronic inflammation. Lipid metabolism plays a central role in this pathology, especially in the setting of elevated low-density lipoprotein cholesterol (LDL-C). Furthermore, the protective capacity of high-density lipoprotein (HDL) is increasingly understood to depend on its functionality rather than absolute levels, as it can become dysfunctional and pro-inflammatory in pathological states. Emerging evidence has identified lipoprotein(a) [Lp(a)] and triglyceride-rich lipoproteins as significant, independent contributors to microvascular injury. Comprehensive clinical assessment of microvascular dysfunction therefore requires integration of advanced lipid profiling, including apolipoprotein B (ApoB), [Lp(a)], and the triglyceride-glucose (TyG) index with invasive and non-invasive measures of coronary flow reserve to more precisely stratify risk. In this narrative review, we synthesize current observational, mechanistic, and early interventional data linking diverse lipid phenotypes to coronary microvascular dysfunction. We propose a concept of lipid-driven CMD endotypes, such as ApoB-/particle overload, dysfunctional HDL, Lp(a)-mediated risk, and metabolic/TyG-high states, and map these to a practical, mechanism-informed management framework. While intensive LDL-C lowering with high-intensity statins and combination therapy remains guideline-directed care for high-risk patients, evidence for dedicated microvascular benefit from newer lipid and cardiometabolic agents is still largely hypothesis-generating. A personalized approach that aligns lipid phenotyping, CMD endotyping, and existing guideline-based therapies may help refine risk assessment and inform future trials. - Source: PubMed
Publication date: 2026/05/06
Hafez AbdelrahmanFarina Juan MAwad KamalPietri Milagros PereyraScalia Isabel GSheashaa HeshamAbdelfattah Fatmaelzahraa ERazaghi MahshadAhmed SherifIbrahim RamziSimper DavidLester Steven JTamarappoo BalajiAyoub ChadiArsanjani Reza - While reducing LDL cholesterol (LDL-C) remains central focuses of conventional preventive cardiology, substantial heterogeneity exists in the cardiovascular risk associated with even extreme LDL-C elevations, likely depending heavily on the broader metabolic context. Specifically, the lean mass hyper-responder (LMHR) phenotype-characterized by markedly elevated LDL-C with elevated high-density lipoprotein cholesterol (HDL-C) and low triglycerides in the setting of a ketogenic diet-has recently been described, though its long-term risk profile remains poorly defined. - Source: PubMed
Publication date: 2026/05/11
Norwitz Nicholas GFeldman DavidSoto-Mota Adrian - Incretin-based therapies have gained momentum as a key strategy for reducing cardiovascular risk in individuals with obesity and/or type 2 diabetes (T2D). It remains unclear whether the cardiovascular benefits reflect a direct reduction in atherogenic lipoproteins-namely, low-density lipoproteins (LDL), very low-density lipoproteins (VLDL) and triglycerides-or broader effects mediated by weight loss, improved insulin sensitivity and reduced ectopic adiposity. This review examines these relationships in depth. We summarise molecular, cellular and physiological evidence describing how GLP-1, GIP, glucagon and amylin signalling regulate intestinal lipid absorption, hepatic apolipoprotein B (apoB)-lipoprotein assembly and peripheral lipoprotein catabolism. These mechanistic insights are integrated with the available clinical data on single or dual GIP/GLP-1 agonists and on related compounds that complement the modulation of either glucagon or amylin. Overall, these therapies predominantly reduce triglycerides and VLDL cholesterol, with these changes closely linked to reductions in hepatic ectopic adiposity and parallelled improvements in glycaemic control, insulin sensitivity and body weight. Agents that additionally activate glucagon or amylin pathways consistently produce greater lipid-lowering effects, supporting the concept that lipid benefits scale with global metabolic reprogramming rather than isolated receptor activation. Despite consistent lipid improvements, the short duration of most clinical trials limits assessment of long-term cardiovascular risk reduction. Moreover, the absence of data on apoB precludes definitive conclusions regarding changes in atherogenic lipoprotein burden. Uncertainty also remains regarding the preservation of lean mass during substantial weight loss. This review provides an up-to-date synthesis linking incretin pharmacology to lipid metabolism and identifies priorities for future cardiometabolic research. - Source: PubMed
Publication date: 2026/05/25
Baragetti AndreaNorata Giuseppe Danilo - There is interest in developing lipoprotein(a) [Lp(a)] lowering therapies. Cholesteryl ester transfer protein inhibitors lower Lp(a), however the effects of the selective inhibitor obicetrapib on Lp(a) levels in high cardiovascular risk patients have not been fully elucidated. This analysis investigated the effect of obicetrapib on Lp(a). - Source: PubMed
Publication date: 2026/05/25
Nicholls Stephen JNelson Adam JRay Kausik KDitmarsch MarcKling DouglasHsieh AndrewSzarek MichaelKastelein John JDavidson Michael H