CLDN1 (Claudin 1)

Respiratory exposure to CD-NPs induces colitis-like lesions via gut microbiota dysbiosis and P53/SCO2/SLC7A11-mediated epithelial ferroptosis, impairing the intestinal barrier. These findings provide new insights into the health risks associated with coal dust exposure.

Furthermore, EGO has been shown to enhance CLDN1 and TJP1 expression (p < 0.05), while significantly reducing OCLN levels (p < 0.05). These findings suggest that, given growth performance, safety, and efficacy, an additive dosage of 200 mg/kg is recommended.

Our findings indicate that TNFRSF21 is a pivotal regulator of epithelial keratinization and tight junction integrity in oral epithelial keratinocytes. Targeting TNFRSF21 may represent a novel therapeutic strategy to restore oral epithelial function.

Notably, CLDND1 :: WRN and DUSP22 :: APOE produced the most pronounced VNC phenotypes. Together, these findings demonstrate that untargeted transcriptome-wide GF discovery, coupled with long-read isoform-level analysis and in vivo functional validation, enables the identification and prioritization of potentially novel and clinically relevant GFs that are missed by standard targeted short-read fusion panels in glioma.

In HT-29 cells, the strains significantly reduced sodium nitroprusside-induced nitric oxide (NO) overproduction, thus indicating their capacity to mitigate nitrosative stress...Mechanistic analyses revealed that these protective effects were associated with the inhibition of nuclear factor-kappa B activation and the suppression of mitogen-activated protein kinase phosphorylation cascades. These findings demonstrate the anti-inflammatory and barrier-protective potential of L. plantarum WB4201, WB4202, and WB4203, thus underscoring their potential as probiotic-based interventions for intestinal health.

In summary, this study suggests that HMOs plus probiotics may alleviate AAD by promoting IAA production via the gut microbiota, thereby activating the IAA/AhR/Muc2/claudin-1 axis. This research provides novel insights into microbiota-based interventions targeting intestinal health.

At the mechanistic level, RKIP upregulation inhibited p42/44 mitogen-activated protein kinase (MAPK) and NF-κB signaling that, in turn, downregulated the expression of the two EMT transcription factors Snail and Slug. Despite these preliminary findings needing to be confirmed in more representative ex vivo (such as patient-derived primary cells or patient-derived organoids) and in vivo TNBC models, they provide evidence that the EMT process could be pharmacologically reverted by the protease inhibitor GM in a highly metastatic TNBC in vitro model, deserving further investigation in future studies.

Drug-gene mapping revealed candidates spanning those already in clinical trials for HNC (e.g., Afatinib, Cabozantinib, Dasatinib, Brigatinib, Lenvatinib, Capivasertib, and Erdafitinib) and emerging or repurposing candidates (Amuvatinib, XL765 (Voxtalisib), Golotimod, Artenimol, Quercetin, and Acetylsalicylic Acid), offering opportunities for precision repurposing...HPV stratification enhances precision, literature-based validation strengthens confidence, and integrated drug mapping enables refinement of existing therapies and discovery of novel candidates for personalized treatment strategies. Code Availability: The full implementation of the GARD pipeline, including preprocessing scripts, statistical analysis modules, and visualization tools, is publicly available on GitHub.

It also modulated bile acid metabolism by elevating the levels of hyodeoxycholic acid (HDCA) and deoxycholic acid (DCA), which ultimately suppressed hepatic lipid synthesis and inflammatory responses. These findings collectively suggest that P-RS exerts protective effects against NAFLD by modulating the gut-liver axis.

Continuous probiotic administration provides critical protection against FLF by fortifying epithelial tight junction integrity, suppressing gut-derived inflammatory signaling, and limiting hepatocellular damage. These findings support the utility of targeted microbiota-directed interventions as adjunctive preclinical therapeutic strategies for acute liver failure and warrant further translational evaluation.

UTI confers broad and integrated protection of the intestine during sepsis. These findings suggest that IL-1β-mediated inflammatory signaling plays a key role in UTI-induced enteric neuroprotection and restoration of intestinal motility.

HDW exerts significant antifibrotic effects in CCl4-induced liver fibrosis via a gut microbiota-dependent mechanism involving the restoration of BA metabolism and the activation of the hepatic FXR/SHP/CYP7A1 axis. Given its ability to modulate gut microbial ecology, BA homeostasis and intestinal barrier integrity simultaneously, HDW is a promising therapeutic candidate for targeting the gut microbiota in the treatment of liver fibrosis.