Ask about this productRelated genes to: SLC22A12 Blocking Peptide
- Gene:
- SLC22A12 NIH gene
- Name:
- solute carrier family 22 member 12
- Previous symbol:
- -
- Synonyms:
- OAT4L, RST, URAT1
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-07-31
- Date modifiied:
- 2016-02-18
Related products to: SLC22A12 Blocking Peptide
Related articles to: SLC22A12 Blocking Peptide
- Hyperuricemia is a metabolic disorder characterized by abnormally elevated blood uric acid levels. Elevated serum uric acid levels can lead to crystal deposition in joints and tissues, causing inflammation and pain characteristic of gout and also contributing to renal dysfunction and vascular complications. It is closely associated with various health issues including gout, kidney stones, chronic kidney disease, and cardiovascular diseases. Understanding the underlying causes of hyperuricemia is critical. This review focuses on the causes of hyperuricemia from several key perspectives: the changes in uricase during evolution and the occurrence of pseudogenic mutations; the impact of uric acid transporters such as SLC22A12, SLC2A9, and ABCG2 on uric acid levels; and summarizes sex-related differences in clinical manifestations and differentially expressed genes. Additionally, it explores the potential mechanisms of uric acid regulation from hormonal, transcription factor, and epigenetic perspectives, integrating the findings from previous studies. By integrating insights from evolutionary biology, genetics, epidemiology, and molecular biology, this review aims to offer a comprehensive framework for understanding hyperuricemia. This highlights the need for new approaches in both research and clinical practice to advance our knowledge of hyperuricemia and improve patient outcomes through innovative diagnostic tools or tailored therapies. - Source: PubMed
Publication date: 2025/12/08
Yang YanJi YuweiZhang ZiyueYang JianChen XiangmeiCai GuangyanHong Quan - Hyperuricemia, characterized by elevated serum uric acid (SUA) levels, is increasingly recognized as a significant contributor to cardiometabolic diseases including hypertension, type 2 diabetes, chronic kidney disease, metabolic syndrome, and atherosclerotic cardiovascular disease. In the past, uric acid was seen mainly as a byproduct of purine metabolism linked to gout. However, growing evidence suggests that it plays an active role in causing metabolic and vascular dysfunction. Mechanistic studies have shown that higher uric acid levels can induce endothelial dysfunction, oxidative stress, inflammation, insulin resistance, and activation of the renin-angiotensin-aldosterone system, which together can worsen cardiometabolic conditions. Recent advances in high-throughput omics technologies have greatly improved understanding of the molecular mechanisms regulating uric acid metabolism. Genome-wide association studies (GWAS) have identified important urate transporter genes like SLC2A9, ABCG2, and SLC22A12, while epigenomic studies reveal how DNA methylation, histone changes, and non-coding RNAs connect genetic factors to environmental influences. Transcriptomic and single-cell RNA sequencing analyses explain how urate transport and inflammatory signaling are regulated in specific tissues, including the kidneys, liver, adipose, and vascular tissue. In parallel, metabolomic and proteomic studies have linked hyperuricemia to disruptions in purine metabolism, redox balance, lipid remodeling, and inflammatory protein networks. Together, multi-omics approaches that integrate genomics, epigenomics, transcriptomics, proteomics, and metabolomics, along with expression quantitative trait locus (eQTL) mapping, causal modeling, network biology, and AI analysis, now provide powerful tools for biomarker discovery and mechanistic interpretation. This review summarizes current insights into uric acid metabolism from a multi-omics perspective and highlights emerging opportunities for better risk assessment, biomarker discovery, therapeutic targeting, and tailored prevention strategies in cardiometabolic disease. - Source: PubMed
Publication date: 2026/05/25
Ali Nurshad - The management of hyperuricemia and gout remains constrained by the narrow therapeutic index of current drugs. To improve the druggability of our previously identified URAT1 inhibitor , we replaced its carboxylic acid with a sulfonamide group. A total of 40 novel derivatives were synthesized, among which 23 derivatives exhibited robust serum uric acid-lowering activity. Lead compound (bearing a -bromobenzenesulfonamide) exhibited potent URAT1 inhibition (IC = 0.19 μM) and significantly lowered serum uric acid in hyperuricemic mice (96.8% reduction) and rats (91.9% reduction). Notably, compound also inhibited IL-1β activity (IC = 3.39 μM), which may enhance its therapeutic potential in gout by targeting disease-associated inflammation. Compound demonstrated favorable pharmacokinetics (half-life: 6.3 h, oral bioavailability: 20.1%) and high safety (MTD > 1000 mg/kg). These results establish compound as a promising dual-acting candidate for gout therapy. - Source: PubMed
Publication date: 2026/05/26
Shi XiaoyuShi ChengYang MingyuYu ZeqiYang QianLiu ZhenmingPang JianxinZhan PengLiu XinyongZhao Tong - Hyperuricemia is a chronic metabolic disorder posing serious health risks. Dendrobium huoshanense stems are widely used as medicine and functional food ingredients, but the leaves remain underutilized, and their health potential remains unexplored. - Source: PubMed
Publication date: 2026/05/22
Han ShuoLi ChengwangZhang JieLuo ShengyongGe RuiqinXu YanZhou XiuhongGong PengLiu Zenghui - Gout and hyperuricemia, caused by high serum uric acid, require safer and more effective treatments due to the toxicity and limited efficacy of current drugs. Dual inhibition of URAT1 and GLUT9 may reduce renal toxicity compared to single-target approaches. Starting from lead compound , we used scaffold hopping and structure-guided design to develop 46 novel polycyclic pyrimidine derivatives. Among these, compound showed potent and balanced inhibition of URAT1 (IC = 4.01 μM) and GLUT9 (IC = 1.60 μM), greatly improving upon . Additionally, reduced serum uric acid levels by 82.4% in hyperuricemic mice, while it exhibited favorable pharmacokinetic profiles in rats ( = 33.71 vs 20.13% for ). Significantly, was efficacious at a low dose (0.5 mg/kg) and showed no acute toxicity at 1000 mg/kg. These results support as a promising dual URAT1/GLUT9 inhibitor with improved efficacy, pharmacokinetics, and safety for treating gout and hyperuricemia. - Source: PubMed
Publication date: 2026/05/06
Yang QianQi DanhuiYe WenjieShi XiaoyuYang MingyuWu TingWu ZhenkunXu YuexinWang YouzhaoXu ShujingWang ZhenqianGao ShenghuaYi FanPang JianxinLiu XinyongZhan Peng