Ask about this productRelated genes to: ApoA1 protein
- Gene:
- APOA1 NIH gene
- Name:
- apolipoprotein A1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: ApoA1 protein
Related articles to: ApoA1 protein
- Osteoporosis is a major health issue that has implications worldwide, both clinically and socioeconomically. Therefore, searching for informative bone health biomarkers that provide early information on bone changes and assess treatment efficacy is essential. Previously, our group used label-free proteomics and bioinformatic approaches to analyze the serum proteomic profile of postmenopausal women with normal bone mineral density (BMD), osteopenia, and osteoporosis. Based on their role in bone metabolism and literature review, a panel of 12 candidate serum biomarkers for low BMD was proposed. - Source: PubMed
Publication date: 2026/08/05
Aparicio-Bautista Diana IBecerra-Cervera AdrianaRivera-Paredez BereniceJiménez-Ortega Rogelio FLópez-Pérez Tania VSalmerón JorgeReyes-Grajeda J PabloHidalgo-Bravo AlbertoVelázquez-Cruz Rafael - This study aims to explore the association of lipid indicators, including LDL-C, HDL-C, TC, lipoprotein a (Lpa), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), and the composite lipid indicator triglyceride-glucose index (TyG), with the risk of osteoporotic fracture. A retrospective analysis was performed based on clinical data from 3 987 patients hospitalized in the Department of Osteoporosis at West China Fourth Hospital, Sichuan University, between December 2017 and October 2024. Based on the presence or absence of osteoporotic fracture, the patients were divided into cases and controls. Logistic regression models, mediation effect models, and stratified analysis were applied to explore the association. The area under the curve (AUC) was used to evaluate the model's prediction performance. Maximum likelihood estimation and targeted maximum likelihood estimation were used under the causal contrast weighting framework for causal inference analysis. The level of HDL-C in the case group was higher than that in the control group, while the opposite was true for the levels of ApoA1 and ApoB (all <0.05). Logistic regression analysis revealed a positive correlation between HDL-C and osteoporotic fracture risk (=1.36, 95%: 1.12-1.66, =0.002), while ApoA1 (=0.76, 95%: 0.64-0.90, =0.002) and ApoB (=0.83, 95%: 0.70-0.98, =0.031) showed a negative correlation with osteoporotic fracture risk. Stratified analysis showed that the effects of HDL-C were mainly observed in elderly patients (≥65 years old), whereas those of ApoA1 and ApoB were mainly observed in elderly and obese patients (BMI≥24.00 kg/m). Mediation analysis showed that HDL-C indirectly affected fractures through femoral neck and lumbar spine bone density (mediation ratios of 21.10% and 22.50%), while LDL-C was mediated by lumbar spine bone density (mediation ratio of 33.40%). After combining HDL-C, LDL-C, ApoA1, and ApoB indicators, the model's AUC increased significantly (=0.010), and its predictive performance improved. Causal inference analysis supported that ApoA1 (maximum likelihood estimation: =0.83, 95%: 0.73-0.92, =0.002; targeted maximum likelihood estimation: =0.81, 95%: 0.72-0.94, <0.001) and ApoB (maximum likelihood estimation: =0.84, 95%: 0.74-0.94, =0.004; targeted maximum likelihood estimation: =0.85, 95%: 0.74-0.96, =0.009) were inversely associated with osteoporotic fracture risk, the association of HDL-C with osteoporotic fracture was only significant in the maximum likelihood estimation model (=1.20, 95%: 1.06-1.40, =0.012). Elevated HDL-C levels were associated with increased risk of osteoporotic fractures, while elevated ApoA1 and ApoB levels were associated with decreased risk, and the association between the latter two was more robust in the causal inference analysis. Lipid indicators are useful for predicting and evaluating osteoporotic fracture risk and have potential clinical value for preventing osteoporotic fracture. - Source: PubMed
Li Z HLiu TPang Y QChen Z LJu YXia H XXia M YZhong Y DFan M YJiang XTian Y R - This study explored the genetic evidence linking triglyceride-related pathways and lipid-lowering drug targets with endometriosis risk and investigated the genetic association between TG levels and EM. Using genome-wide association study (GWAS) data, a two-sample Mendelian randomization (MR) analysis was conducted, estimating the association between genetically predicted TG levels and EM risk (OR = 1.1853, 95% CI: 1.070-1.313, p = 0.0011). Seven TG-lowering drug target genes (SLC9A1, SCN3A, VEGFA, APOA1, TNF, ITGAV, BACE1) were identified. Transcriptome analysis revealed that SCN3A, BACE1, and APOA1 were significantly upregulated in EM patients compared to healthy controls. Enrichment pathway analysis showed that these genes are involved in lipid transport, localization, cell adhesion, and blood vessel development. PPARA was predicted to act as a transcription factor for five of these genes, while estrogen receptor 1 (ESR1) was predicted to regulate the majority of the others. Among the TG inhibitors examined, fibrate-related targets showed relatively broader target coverage in the present genetic analyses. These findings suggest that TG-related pathways and lipid-lowering drug targets, particularly fibrate-related targets, may be relevant to EM biology and warrant further experimental and clinical validation. - Source: PubMed
Publication date: 2026/08/13
Li YonghongHe JiananZhang YuanqingYang MinJia ZhimaoFan YidanLiu ShuyunQi Mengsha - Reverse cholesterol transport by HDLs (high-density lipoproteins) is considered an antiatherogenic metabolic pathway. Hepatocytes are the main contributors to the efficacy of this pathway by the production of apoA-I (apolipoprotein A1) and its lipidation by ABCA1 (ATP-binding cassette transporter A1), selective uptake of cholesterol via SR-BI (scavenger receptor class B type 1), and uptake of entire HDL particles. The molecular determinants of the latter step are not well understood. - Source: PubMed
Publication date: 2026/08/13
Panteloglou GrigoriosZanoni PaoloLaw Christopher SWoods BrianOthman AlaaYalcinkaya MustafaNorrelykke Simon FRzepiela Andrzej JStoma SzymonStebler MichaelKerksiek AnjaVisentin MicheleSmit MariekeWolters Justina ClarindaKakava SofiaPotapenko AntonSchlumpf EvelineRadosavljevic SilvijaHäusler StephanieFutema MartaDalila NawarTybjaerg-Hansen AnneHumphries Steve EKuivenhoven Jan AlbertSluis Bart van deLütjohann DieterMeier RogerRobert JérômeChou JanetGeha Raif SShum Anthony KRohrer Luciavon Eckardstein Arnold - Inherited retinal degeneration (IRD) comprises a genetically heterogeneous group of disorders in which the mechanisms linking genetic variation to molecular heterogeneity remain poorly understood. Here, we investigated the contribution of lipid and retinoid metabolism to the molecular etiology of IRD through an integrative analysis of proteomic and biochemical data. A cohort of 203 patients with inherited retinal degeneration was genetically characterized by whole-exome sequencing (WES), followed by targeted profiling of lipid-related proteins, including apolipoprotein A1 (ApoA1), apolipoprotein E (ApoE) and lipoprotein lipase (LPL), together with the quantitative assessment of systemic lipid parameters. Integrative analyses identified a coordinated lipid-retinoid-photoreceptor metabolic network linking systemic lipid metabolism with photoreceptor-associated processes. Although conventional lipid measures largely remained within clinical reference ranges, their distributions revealed substantial biological variability. Lipid-associated network architecture defined distinct patterns of molecular organization and exhibited pronounced sex-dependent differences, with female patients displaying denser and more interconnected networks than male patients. Furthermore, the integration of genetic and protein expression demonstrated that variant pathogenicity is associated with the coordinated remodeling of lipid-related molecular states. Our findings identify lipid and retinoid metabolism as integral components of the molecular architecture underlying disease heterogeneity in IRD and reveal a lipid-retinoid metabolic network linking genetic variation to coordinated molecular remodeling. These results provide new insight into the molecular mechanisms contributing to photoreceptor-associated degeneration. - Source: PubMed
Publication date: 2026/08/01
Sołek PrzemysławCholewińska EwelinaRejdak RobertNowomiejska KatarzynaOgnik Katarzyna