Ask about this productRelated genes to: TLR9 Blocking Peptide
- Gene:
- TLR9 NIH gene
- Name:
- toll like receptor 9
- Previous symbol:
- -
- Synonyms:
- CD289
- Chromosome:
- 3p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-10-05
Related products to: TLR9 Blocking Peptide
Related articles to: TLR9 Blocking Peptide
- Aberrant changes in circulating cell-free mitochondrial DNA (ccf-mtDNA) across gestation are associated with adverse pregnancy outcomes. Given the inflammatory properties of ccf-mtDNA via pattern recognition receptors such as Toll-like receptor 9 (TLR9), we hypothesized that extracellular mtDNA induces placental inflammation via TLR9 signaling and that this response differs by fetal sex. Pregnant Sprague-Dawley rats were treated intravenously with purified mtDNA (300 μg/kg), nuclear DNA (nDNA), saline, and/or the TLR9 antagonist ODN2088 across five studies. Placental responses were evaluated 4 h (Studies 1-3) and 24 h (Study 4) post-treatment; pregnancy and neonatal outcomes were assessed at delivery (Study 5). Exposure to mtDNA, but not nDNA, increased placental , , and mRNA (p < 0.05), establishing response specificity. mtDNA-induced placental inflammation was fetal sex-dependent: mtDNA increased and mRNA in male placentas (p ≤ 0.0004) but not female placentas, whereas was selectively induced in female placentas (p = 0.0004). TLR9 and MyD88 abundance increased in female but not male placentas, and TLR9 antagonism modified selected inflammatory responses with sex-specific patterns. The 4 h inflammatory transcriptional signature resolved by 24 h, whereas mtDNA exposure was associated with a sex-specific shift in antioxidant enzyme expression persisting to 24 h. Despite no effects on gestational length or neonatal biometrics, mtDNA exposure was associated with a higher estimated stillbirth count per litter (IRR = 4.23, 95% CI [0.89, 20.1], p = 0.069). These findings establish extracellular mtDNA as an acute, sex-differentiated placental inflammatory stimulus with partial TLR9 dependence and a potential impact on fetal viability. - Source: PubMed
Publication date: 2026/07/11
da Silva Reneé de Nazaré OliveiraHula NataliiaEscalera DesiraeLopez LeslieKelly GabrielleGorham Isabelle KRowe MeganRicci Contessa AGheorghe CiprianPhillips Nicole RGoulopoulou Styliani - Aging is among the major risk factors for male infertility. Coridius chinensis is a traditional Chinese insect medicine that has been utilized to improve male reproduction in China for hundreds of years, but elucidation of the underlying mechanisms involved remains challenging. - Source: PubMed
Publication date: 2026/07/08
Zhang MeiZeng FengyinLou HuixianMa JingHou Xiaohui - Immunoglobulin A (IgA) nephropathy is a systemic immune complex-mediated disease primarily affecting the kidneys, yet pulmonary involvement remains poorly characterized. This study investigated pulmonary structural alterations, IgA deposition, immune cell distribution, and the impact of chronic environmental immune stimulation. - Source: PubMed
Publication date: 2026/07/16
Kim AreumLee MinhyeokPark YohanHwang Wan JinLee HyeseungKim Joo HeonKim Jin ManKim Yong MinPark Jin SunLee Junguee - This study focuses on the synthesis of glucovanillin mediated by UGT109A1 and its mechanism against Type 2 Diabetes Mellitus (T2DM). Recombinant UGT109A1 successfully synthesized glucovanillin from vanillin using UDP-Glc as the sugar donor. Through network pharmacology, 140 potential targets were identified. Seven key targets were further screened using LASSO and SVM-RFE algorithms. Among these, SLC5A1 and ADK showed strong diagnostic potential, with AUC values ranging from 0.85 to 0.89. Immune infiltration analysis linked these core targets to M2 macrophages. Single-cell transcriptomics revealed that ADK is widely expressed but enriched in B cells, while TLR9 is confined to plasmacytoid dendritic cells (pDCs). Cell-to-cell communication analysis identified a pDC-to-B cell signaling axis. In vitro assays demonstrated that glucovanillin exhibits concentration-dependent inhibitory activity against α-glucosidase with moderate potency, with an IC of 413.84 ± 12.80 μM. Molecular docking, 200 ns molecular dynamics simulations (MD), and MM/PBSA calculations showed that glucovanillin binds more strongly to α-glucosidase (-7.4 kcal/mol) than vanillin (-5.4 kcal/mol). Therefore, the glycosylation mediated by UGT109A1 enhanced the bioactivity and targeting specificity of vanillin. In summary, glucovanillin exerts anti-T2DM effects through a dual mechanism involving α-glucosidase inhibition and regulation of key targets, making it a promising lead compound for T2DM treatment. - Source: PubMed
Publication date: 2026/06/24
Zhang HuanyuZhang WeiqianLi FangyaLu XinyaoYan YupingZhang Dan - Sepsis is a life-threatening syndrome characterized by a dysregulated host response to infection and progressive organ dysfunction. Although early antimicrobial therapy, source control, hemodynamic resuscitation, and organ support remain the foundations of care, these approaches do not directly reverse the cellular mechanisms that connect systemic inflammation to multi-organ failure. Mitochondrial dysfunction has emerged as a central mechanism linking impaired oxygen utilization, oxidative and nitrosative stress, immune-cell metabolic reprogramming, inflammatory amplification, and organ injury. During sepsis, inflammatory mediators, nitric oxide, microcirculatory abnormalities, calcium dysregulation, and metabolic stress converge on mitochondria, impairing oxidative phosphorylation and promoting mitochondrial reactive oxygen species/reactive nitrogen species (ROS/RNS) generation. When mitochondrial quality-control programs, including fission, fusion, mitophagy, and mitochondrial biogenesis, fail to restore network integrity, damaged mitochondria accumulate and become persistent sources of oxidative stress and danger signals. Mitochondrial damage-associated molecular patterns, particularly mitochondrial DNA, oxidized mitochondrial DNA, cardiolipin, ATP, and N-formyl peptides, activate innate immune pathways such as TLR9-MyD88-NF-kappaB, the NLRP3 inflammasome, and cGAS-STING signaling. In parallel, mitochondrial metabolism shapes macrophage activation, neutrophil function, T-cell competence, pyruvate-lactate handling through the pyruvate dehydrogenase complex, and the transition between hyperinflammation and immunosuppression. Clinical translation remains challenging because sepsis is biologically heterogeneous and mitochondrial dysfunction is dynamic, tissue-specific, and influenced by disease stage. This review synthesizes current knowledge on mitochondrial dysfunction in sepsis, emphasizing oxidative and nitrosative stress, mitochondrial quality control, mitochondrial damage-associated molecular pattern (DAMP) signaling, immunometabolism, organ-specific injury, candidate biomarkers, clinical translational strategies for mitochondria-targeted therapy, and future approaches based on multi-omics and artificial intelligence-assisted patient stratification. We argue that future therapeutic development should move beyond nonspecific antioxidant supplementation toward time-sensitive, phenotype-informed, and biomarker-guided mitochondrial medicine. - Source: PubMed
Publication date: 2026/06/30
Kim MinsooKhin Phyu PhyuJung HyeranChae Chang WooJeon Byeong HwaKim Cuk-Seong