Ask about this productRelated genes to: ApoB protein
- 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 protein
Related articles to: ApoB protein
- Despite significant breakthroughs in preventative medicine, atherosclerotic cardiovascular disease (ASCVD) is still the primary cause of morbidity and death worldwide. In this context, 2 apoB-containing particles-LDL and lipoprotein(a) [Lp(a)] have emerged as important but mechanistically separate causes of atherothrombotic illness. This review synthesizes current knowledge in lipid biology, epidemiology, measurement, and therapeutics to address 3 key questions: (1) how LDL-C/apoB and Lp(a) differ in structure, pathophysiology, and clinical risk; (2) what the evidence shows about the safety and efficacy of driving LDL-C to very low or near-zero levels; and (3) where PCSK9-based therapies and soon, dedicated Lp(a) -lowering agents-fit into modern prevention strategies. Randomized trials, MR studies, and population-level cohort data all contribute to a clear and convincing picture: LDL-C/apoB and Lp(a) are separate causative drivers of cardiovascular risk, with Lp(a) introducing an orthogonal risk axis determined by genetics rather than lifestyle. By combining both viewpoints, we propose a feasible, dual-axis strategy to ASCVD prevention that addresses both cumulative apoB load and genetically driven Lp(a) risk. - Source: PubMed
Publication date: 2026/09/23
Anamika FnuDawar PrachiAggarwal KanishkDixit SakshiKugalur Saravanan GowrisankarNanjundappa Aravinda - The lean mass hyper-responder (LMHR) phenotype describes marked increases in low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (ApoB) during carbohydrate-restricted ketogenic diets, usually in lean, metabolically healthy individuals with high high-density lipoprotein cholesterol and low triglycerides. - Source: PubMed
Publication date: 2026/09/11
Lechner BenjaminLechner KatharinaRubinstein GermanParhofer Klaus GVogt Anja - Abnormal tumor vasculature, hypoxia, altered lipid use, oxidative-matrix injury, and immune remodeling often coexist, but their spatial and causal relationships remain incompletely resolved. We examine whether vascular boundary failure can pathologically relocate circulating apolipoprotein B (ApoB)-containing triglyceride-rich lipoproteins (ApoB-TRLs) into the tumor interstitium and thereby create a focal source of free fatty acid (FFA)-linked injury. - Source: PubMed
Publication date: 2026/09/22
Liu YuwuShi Ping - Exposure to per- and polyfluoroalkyl substances (PFAS) and heavy metals may be associated with dyslipidemia. However, evidence regarding the joint associations and potential interactions of these pollutants remains limited, and the biological pathways that might be relevant to these associations are not yet fully understood. This study, conducted in three communities in Guangzhou, China involving 1310 participants during 2018 to 2019, investigated the associations between co-exposure to serum PFAS (detection frequency over 85%) and three plasma heavy metals (arsenic (As), lead (Pb), and cadmium (Cd)) with dyslipidemia. Bioinformatic approaches were used to identify candidate biological processes potentially related to these associations. The results showed that individual PFAS, As, and Cd were positively associated with dyslipidemia. Furthermore, the Grouped Weighted Quantile Sum (GWQS) regression model indicated that co-exposure to PFAS and heavy metals was positively associated with dyslipidemia (odds ratio (OR) = 2.19, 95% confidence interval (CI): 1.80, 2.68). Significant additive interaction effect was observed between perfluoro-n-nonaoic acid (PFNA) and Cd for dyslipidemia, with the low-exposure group for both pollutants as reference (relative excess risk due to the interaction (RERI) = 1.21, 95% CI: 0.39, 2.02). A total of 110 overlapping genes associated with PFAS, Cd, and dyslipidemia were identified. KEGG enrichment analyses highlighted PPAR signaling pathway, cholesterol metabolism, insulin resistance, AMPK signaling pathway, and adipocytokine signaling pathway as candidate biological processes shared among PFAS, Cd exposure, and dyslipidemia. Subsequent six hub genes (PPARA, PPARG, APOB, APOE, INS, and SREBF1) were screened using Cytoscape. These findings provide new insights into the associations between multiple pollutants co-exposure with human health and identify potential biological pathways for future mechanistic investigation. - Source: PubMed
Publication date: 2026/09/22
Fan Yuan-YuanLin Li-ZiAmjad MuhammadZhou YangChu ChuGui Zhao-HuanBao Wen-WenHuang Jing-WenLiang Li-XiaZhang Yun-TingZhao KunLiu XuanChen Yan-XuDong Guang-HuiHu Li-Wen - The use of BPA alternatives in consumer products has increased substantially, yet their long-term metabolic safety remains poorly understood. This study investigated the effects of perinatal exposure to bisphenol AP (BP-AP) on multigenerational metabolic and cardiovascular outcomes, with particular emphasis on cholesterol homeostasis in hepatic and cardiac tissues and the potential association between hepatic and cardiac alterations. F0 dams were exposed to BP-AP during gestation and lactation, and metabolic phenotypes were evaluated in F1 and F2 offspring. Oral glucose tolerance and insulin tolerance tests were performed to assess glucose homeostasis, while echocardiography was used to evaluate cardiac structure and function. Histopathology, serum lipid profiling, urine metabolomics, oxidative stress assessments, and gene and protein expression analyses were conducted to investigate molecular and metabolic alterations associated with BP-AP exposure. Both F1 and F2 male offspring exhibited impaired glucose homeostasis and progressive cardiac dysfunction, characterised by increased left ventricular mass, reduced ejection fraction, and myocardial histopathological abnormalities. Urine metabolomics revealed elevated hydroxycholesterol species, consistent with altered cholesterol turnover. Hepatic and cardiac tissues showed increased cholesterol accumulation, accompanied by altered estrogen receptor signalling and activation of the SREBP2-HMGCR cholesterol biosynthetic pathway. Genes involved in cholesterol uptake, transport, and reabsorption, including LDLR, SR-B1, NPC1L1, APOA1, and APOB, were dysregulated, together with compensatory changes in cholesterol efflux transporters. BP-AP exposure also induced persistent oxidative stress, as evidenced by increased oxidative damage biomarkers and cardiac malondialdehyde levels, together with reduced glutathione and catalase activities. These molecular alterations were more pronounced in males and persisted across generations. In conclusion, perinatal BP-AP exposure was associated with multigenerational, sex-specific disruption of cholesterol homeostasis in hepatic and cardiac tissues, oxidative stress, and cardiometabolic dysfunction. The coordinated hepatic and cardiac alterations suggest a potential association between disrupted hepatic cholesterol metabolism and cardiac dysfunction. These findings support further investigation of the long-term, multigenerational, and sex-specific biological effects of BPA substitutes. - Source: PubMed
Publication date: 2026/09/22
Pulimamidi Sai SharanyaSingh JayaM SuryaprakashMungase SurajMounika NadellaMalladi NavyaAli AzeemPrakash PremBalani Jagdish KumarAdela RamuBanerjee Sanjay KBorkar Roshan M