Ask about this productRelated genes to: PON1 antibody
- Gene:
- PON1 NIH gene
- Name:
- paraoxonase 1
- Previous symbol:
- PON
- Synonyms:
- ESA
- Chromosome:
- 7q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: PON1 antibody
Related articles to: PON1 antibody
- Hepatocellular carcinoma (HCC) is driven by extensive metabolic reprogramming, vascular remodeling, and immune microenvironmental dysfunction. Although numerous stratification signatures have been proposed, few are grounded in clinically derived serum multi-omics and biologically linked to endothelial remodeling, endothelial regulation, and immune exclusion. - Source: PubMed
Publication date: 2026/08/31
Yang LuxiJin QiaoyingChen LuLiu YatingLi Yumin - Enzyme paraoxonase 1 () plays a protective role against atherosclerosis by preventing the oxidation of low-density lipoproteins (LDL). Polymorphisms in the , particularly Q192R and L55M, have been shown to affect the enzyme activity and, consequently, the cardiovascular risk. The present study aimed to evaluate the association between haplotypes comprising the Q192R and L55M polymorphisms and the severity of coronary atherosclerosis in a Polish population. The retrospective study involved 282 individuals of both sexes, divided into two groups following coronarography. The study group included patients after PCI (percutaneous coronary intervention) with stent implantation or patients who qualified for CABG (coronary artery bypass graft), with stenoses of minimum 70% ( = 140), whereas the control group included those after coronarography and without essential lesions in coronary vessels ( = 142). The Q192R polymorphism was identified by PCR-RFLP. The haplotypes 192R-55L and 192R-55M have been shown to be statistically significantly associated with a higher risk of atherosclerosis that requires PCI/CABG (OR = 2.06, 95% CI: 1.29-3.28, = 0.0022; OR = 1.77, 95% CI: 1.17-2.69, = 0.007; respectively). Furthermore, the risk of atherosclerosis requiring PCI or CABG was 53% lower in patients with the 192Q-55L haplotype (OR = 0.47, 95% CI: 0.34-0.66, = 0.000013). Haplotypes 192R-55L and 192R-55M may increase the risk of atherosclerosis requiring PCI/CABG, whereas the 192Q-55L haplotype may lower the risk. - Source: PubMed
Publication date: 2026/08/14
Rychlik-Sych MariolaBarańska MałgorzataDudarewicz MichałOwczarek Jacek - High-density lipoprotein (HDL)-associated paraoxonase-1 (PON1) contributes substantially to the antioxidant and anti-inflammatory functions of HDL. Impairment of these protective properties has been associated with Alzheimer's disease (AD) and other forms of dementia, particularly those involving neurovascular dysregulation. In the present study, we investigated for the first time the potential involvement of the putative physiological lactonase activity of PON1 in serum samples from a large cohort of older adults (n = 691), including cognitively healthy controls and patients with mild cognitive impairment (MCI), AD, vascular dementia (VAD), mixed AD/VAD (MIXED dementia), and other forms of dementia. A difference was observed between controls and MCI patients (-34%, < 0.001). The next largest differences were observed in the VAD and MIXED dementia groups, both showing a decrease of approximately 25% compared with controls ( < 0.05 and < 0.001, respectively), and in AD patients (-14%, < 0.05). After adjustment for confounding factors, only MCI and MIXED dementia remained significantly different from controls. These findings suggest that reduced serum PON1 lactonase activity is already detectable at the MCI stage and is particularly evident in conditions combining neurodegenerative and vascular pathology. Longitudinal studies are required to determine whether lower PON1 lactonase activity precedes, accompanies, or follows cognitive decline. - Source: PubMed
Publication date: 2026/08/13
Riccetti RaffaellaTrentini AlessandroMola GianmarcoBrombo Gloriadi Paola Dario FrancescoCastellazzi MassimilianoCandeloro RaffaellaManfrinato Maria CristinaZuliani GiovanniCervellati Carlo - : Clinical outcomes after traumatic brain injury (TBI) remain difficult to predict, highlighting the need for more sensitive diagnostic and prognostic biomarkers, particularly in polytrauma. This study aimed to identify TBI-specific proteomic signatures in plasma and extracellular vesicles (EV)-enriched fractions of critically injured trauma patients. : Seventy-five severely injured adult trauma patients (ISS ≥ 16) were included: isolated severe TBI (TBI; AIS ≥ 4, other AIS ≤ 1, = 23), polytrauma with TBI (PT-TBI; AIS ≥ 4, = 22), and polytrauma without TBI (PT; AIS = 0, = 30). 24 age- and sex-matched healthy volunteers served as controls. Neat plasma and EV-enriched fractions were profiled using HPLC-MS/MS. Differentially expressed proteins (DEP) were analyzed bioinformatically, and associations with clinical parameters were assessed using Spearman's correlation. : The EV-enriched plasma fraction yielded more DEPs than neat plasma (846 vs. 258). Most DEPs were linked to polytrauma, with plasma reflecting metabolism and EVs showing translation and protein catabolism signatures. Among TBI-context proteins, EV-associated NRCAM and AQR and plasma IGHV1-69D, MASP1, PON1, and IGFBP7 remained significantly associated with TBI after adjustment for confounder. Notably, only EV-associated proteins correlated with injury-related clinical parameters. AQR negatively correlated with GCS ( = -0.51, < 0.0001), while elevated NRCAM, AQR, and plasma MASP1 were associated with neurological deterioration and neurosurgical intervention. : EV-enriched plasma proteomics enhances biomarker discovery in polytrauma, revealing distinct pathways and greater sensitivity than whole plasma. While most changes reflect systemic injury, EV-associated NRCAM and AQR, along with plasma MASP1, show TBI-specific associations with neurological status, highlighting their potential as candidate TBI biomarkers for further study. - Source: PubMed
Publication date: 2026/07/25
Leppik LiudmilaWeber BirteSchindler Cora RFunda LouiseKrüger MarcusProschinger SebastianHenrich DirkMarzi Ingo - Hypoxic pulmonary hypertension (HPH) is characterized by excessive proliferation of pulmonary vascular cells, ultimately resulting in right heart failure and death. Although resveratrol, an active component of Polygonum cuspidatum (PC), has shown efficacy against HPH, the mechanism of PC exosome-like nanovesicles (PCELNs) in HPH remains unclear. PC exosome-like nanovesicles (PCELNs) were characterized using transmission electron microscopy, dynamic light scattering, and immunofluorescence (IF). A mouse HPH model was established by chronic hypoxic exposure. Hemodynamic parameters were measured, and pulmonary vascular pathology was assessed via H&E and Masson staining. Protein expression of PCNA, α-SMA, and OPN was analyzed by immunohistochemistry (IHC) and IF. Mouse primary PASMCs were isolated and cultured. Cell proliferation, apoptosis, and migration were evaluated using EdU assay, flow cytometry, and Transwell assay, respectively. Proteins related to phenotypic switching, autophagy, and the MAPK pathway were detected via Western blot. JC-1 staining, Mito-Tracker staining, IF, ATP/SOD assay kits, and flow cytometry were used to assess mitochondrial membrane potential, morphology, mitophagy, energy metabolism, and reactive oxygen species levels, respectively. Network pharmacology screened common targets of resveratrol and pulmonary hypertension, with molecular docking validating binding affinity. PC exosome-like nanovesicles (PCELNs) alleviated HPH, significantly improving pulmonary artery remodeling and hemodynamic indices in mice, inhibiting abnormal PASMC proliferation and migration, promoting apoptosis, and ameliorating mitochondrial function. The mechanism involves stabilizing paraoxonase 1 (PON1) expression, thereby suppressing MAPK pathway activation. PC exosome-like nanovesicles (PCELNs) alleviate HPH by enhancing PASMC phenotypic switching and mitigating mitochondrial dysfunction through the PON1/MAPK axis, providing a novel therapeutic strategy. - Source: PubMed
Chen BingchenHu JunfengPan XiaxiaFan RuiChen Chun