Ask about this productRelated genes to: LRAT antibody
- Gene:
- LRAT NIH gene
- Name:
- lecithin retinol acyltransferase
- Previous symbol:
- -
- Synonyms:
- LCA14
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-16
- Date modifiied:
- 2017-08-04
Related products to: LRAT antibody
Related articles to: LRAT antibody
- Given the significant efficacy of the Punica granatum in enhancing skin health, this research employed network pharmacology and in vivo studies to explore the P. granatum ethanolic leaf extract's (PGEL) mechanism in alleviating skin sclerosis. A model of skin fibrosis brought on by bleomycin (100 µl/rat, sc.) was adopted for experimental validation, where PGEL was orally administered at 200 and 400 mg/kg to rats for 3 weeks. Seventy-three compounds of PGEL were identified by LC/MS/MS belonging to different chemical classes; an organic acid, 12 phenolic acids, 4 polysaccharides, 3 amino acids, 19 gallic acid derivatives,7 ellagic acid derivatives, 14 flavonoides, three anthocyanins, 3 fatty acids and 7 miscellaneous groups. Five compounds (Catechin-3-O-gallate, 3,3'-di-O-methyl-4-O-(xylopyranosyl) ellagic acid, ellagic acid glucoside, valoneic acid dilactone, and vitexin 2-O-gallate) were isolated from the PGEL. Network pharmacological studies clarified that TNF-α, TGF-β1, Snail1, p-Smad3, MMP-9, IL-17 A, and COL1A1 are the core targets for skin fibrosis. PGEL lessened MPO and increased SOD activity in rat's skin, underscoring its antioxidant activity. Furthermore, the TNF-α, IL-17 A and MMP-9 were decreased in PGEL groups. Mechanistic studies revealed that PGEL exerts its anti-fibrotic action by downregulating the TGF-β1, Snail 1, COL1A1, and p-Smad 3 in the skin tissues. Additionally, histopathological analyses informed the decline in dermal alterations and thickness in rats treated with PGEL. Collectively, our results give clear evidence that PGEL work through multi-pathway modulation by targeting the core proteins of inflammation mediated the TGF-β/Snail1/Smad 3 signaling, thereby exerting a therapeutic action on skin fibrosis. - Source: PubMed
Publication date: 2026/04/27
Baraka Sara MEl-Gendy Zeinab AEl-Abd Eman A WEl-Sayed Ahmed FOmara Enayat AElbatanony Marwa M - Ozone (O) is a pivotal trace gas at the core of the Earth's coupled climate-chemistry-biosphere system with significant implications for global public health, ecosystem stability, and the Earth's radiative balance. This study integrates a high-density surface O monitoring network deployed along key inflow corridors in the southwestern Tibetan Plateau (TP), with EAC4 reanalysis and Lagrangian transport diagnostics to quantify the contributions of different mechanisms driving summertime surface O formation. By applying an iterative discrete wavelet transform (IDWT), we decompose hourly O concentrations into intra-day (∼8 h), synoptic (1-2 days), and seasonal (∼4 months) components, corresponding to local photochemical production, regional transport, and a quasi-constant background. Results show that regional transport accounts for approximately 78% of the total surface O during the monsoon season (June-September 2024). Decomposition further indicates that, beyond a relatively constant background, stratospheric intrusion (SI) is the primary driver during polluted days (MDA8 O > 160 μg/m), contributing 50.2% to surface O exceedances, followed by long-range anthropogenic transport (LRAT) (28.7%) and local production (LP) (21.1%). Dry conditions and enhanced solar radiation act as critical local amplifiers of O pollution over the plateau. A representative event from 11 to 14 June 2024 reveals a dual-channel "stratosphere-monsoon superposition" mechanism: a descending stratospheric O plume entering from northern Xinjiang superimposes on a monsoon-transported South Asian pollution plume crossing the Himalayas, producing widespread exceedances of 160 μg/m across all surface sites in southwestern TP. Weighted airflow trajectories combining observations and simulations identify that the upwind regions along the northern South Asian pollution belt as primary potential source areas. These findings challenge the notion of the southwestern TP as a predominantly natural O background, instead considering it as a dynamic mixing gateway where stratospheric air and monsoon outflow mix and interact to shape surface oxidant levels. - Source: PubMed
Publication date: 2026/04/15
Chen WenlinQin XiaoliangTao ShikangWang YanyuWang YingYuan ZibingZhuoga SuonaZhang HuifangFu QingyanNing Zhi - Diabetic Retinopathy (DR) is a leading cause of permanent blindness due to the difficulty of early screening. In this context, deep-learning-based automatic DR grading has the potential to significantly improve the diagnostic efficiency of ophthalmologists. However, accurate DR grading remains challenging due to intra-class variations and small lesions. To address this problem, a Lesion Learning Network with a Relation Aware Transformer (LLNet) is proposed in this paper to achieve precise DR grading. Specifically, a Lesion Information Extractor (LIE) is designed to recognize DR-related lesions and extract their fine-grained features through lesion annotations training or lesion-based contrastive learning. Then, the Lesion Saliency Transformer (LST) captures a discriminative lesion-salient sequence by interactively fusing LIE-extracted lesion features with self-attention features, thereby enhancing the perception of small lesions. Finally, the Lesion Relation Aware Transformer (LRAT) is proposed to establish an efficient relational model between DR lesion conditions and severity grades, thereby improving robustness to intra-class lesion variations and enabling more accurate grading predictions. Moreover, an adaptive lesion-learning strategy is designed for LLNet to conduct image-level learning and lesion-annotation-guided learning, thereby facilitating efficient utilization of DR data for generalization. Precision comparison experiments were conducted on the FGADR, DDR, and APTOS datasets. The proposed LLNet achieved accuracies of 82.7%, 86.1%, and 87.2%, respectively, surpassing comparative methods. Furthermore, the superior generalization capability of LLNet was validated by training on the DDR dataset and testing on the EyePACS dataset, achieving an accuracy of 72.1%. - Source: PubMed
Publication date: 2026/04/10
Liang HaoHe ZhaoshuiLin ZhijieSu WenqingGuo JingWang YunxianLiang Jixing - Hepatic stellate cell (HSC) activation is central to liver fibrosis, but emerging evidence suggests HSC homeostatic activity. We compared HSC functions in parenchymal injury (CCl 4 -driven) versus metabolic dysfunction-associated steatohepatitis (MASH; choline-deficient, high-fat diet-CD-HFD) and identified therapeutic targets preserving HSC homeostatic functions. - Source: PubMed
Publication date: 2026/03/19
Yang AitingYan XuzhenWang YiwenHan QiTong XiaofeiChen ShuyanZhao XinyuChen WeiJia JidongSchuppan DetlefYou Hong - Vitamin D deficiency (VD-deficiency) has been implicated in various autoimmune diseases, including uveitis, yet its mechanistic role remains unclear. Emerging evidence suggests that gut microbial dysbiosis and metabolic disturbances may serve as critical intermediates linking VD-deficiency and autoimmune disease pathogenesis. Here, using an experimental autoimmune uveitis (EAU) model induced in B10RIII mice, we demonstrate that VD-deficiency exacerbates EAU severity, accompanied by enhanced Th1 and Th17 responses, suppressed regulatory T cells, and disruption of both intestinal and blood–retinal barrier integrity. Integrated microbiota and metabolomic profiling revealed a coordinated pattern of gut dysbiosis, characterized by enrichment of opportunistic pathogens and depletion of beneficial commensals, together with host metabolic reprogramming in VD-deficient EAU mice. KEGG analysis highlighted disruption of vitamin-related pathways, particularly the pathway. Mechanistically, VD-deficiency associated disturbances were linked to LRAT downregulation in retinal pigment epithelial (RPE) cells, accompanied by a pro-inflammatory intraocular microenvironment characterized by increased IL-6 and CXCL family chemokines expression. Gain- and loss-of-function studies in complementary in vivo and in vitro RPE-based models further demonstrated that LRAT functions as a negative regulator of retinal inflammatory responses, with LRAT knockdown enhancing, whereas LRAT overexpression suppressing, the production of IL-6, CXCL1, CXCL2, and CXCL8. Collectively, our findings suggest that VD-deficiency exacerbates autoimmune uveitis by disrupting effector–regulatory T cell balance and compromising blood–retinal barrier and intestinal integrity, accompanied by considerable alterations in gut microbiota and systemic metabolism, while identifying LRAT as a potential regulator linking VD-deficiency to retinal inflammatory amplification. - Source: PubMed
Publication date: 2026/03/11
Chen ZhijunZhang WanyunDeng YangZhang YinanSu GuannanWang YaoYang Peizeng