CLDN5 (Claudin 5)

Furthermore, CLDN5 knockdown directly impaired endothelial barrier function. Our findings identify CLDN5 as a promising circulating biomarker for TAAD diagnosis and provide new insights into TAAD pathogenesis, offering potential diagnostic strategies.

Furthermore, they acted together on the p38 mitogen-activated protein kinase (MAPK) signaling pathway, and the addition of the p38 inhibitor SB203580 partially inhibited the expression of p38MAPK. Thus, the combined action of these drugs protected the NVU.

A genetic diagnostic model constructed based on ten genes (RIF1, GDPD5, DBNDD1, RCCD1, CLDN5, ASCL2, IFITM3, IFITM1, SMPDL3A, and SUCLG2) demonstrates strong predictive performance. This model holds significant potential for the early diagnosis and intervention of colorectal cancer, contributing to the implementation of third-tier prevention strategies.

Furthermore, both individual and combined modulation of MSI2 knockdown, LINC00667 knockdown and IRF6 over-expression enhanced BTB permeability to doxorubicin (Dox), thereby increasing the apoptosis rate of GB cells. Collectively, the MSI2/LINC00667/IRF6 pathway plays an important role in modulating BTB permeability, offering potential targets for new molecular therapies in GB.

Established therapies such as trastuzumab, pertuzumab, trastuzumab/pertuzumab, lapatinib and tucatinib are widely used and are selectively toxic to HER2-positive breast cancer cell line. In conclusion, we demonstrate different time- and concentration-dependent effects of anti-HER2-targeted therapies for the treatment of advanced HER2-positive breast cancer on the BBB in vitro. Further experiments are required to assess the clinical relevance of our results.

EA at GV24 and GV20 can improve learning memory function in MCAO/R rats, and its mechanism may be related to the repair of the central blood-brain barrier, reduction of pro-inflammatory cytokine levels, and inhibition of microglial activation and central neuroinflammation.

The cholesterol-lowering drug atorvastatin reverses these tumor-intrinsic and microenvironmental effects and suppresses LUAD brain metastasis in vivo. Retrospective clinical analyses further show that hypercholesterolemia is associated with shortened survival in LUAD-BM patients, whereas statin use correlates with improved outcomes. These findings identify cholesterol as a functional mediator downstream of lipid-metabolic dysregulation and therapeutic target in LUAD-BM.

These internalized sEVs were predominantly targeted to lysosomes. Despite severe barrier disruption due to OGD transcellular permeation of single sEV particles was not detectable.

Notably, molecular docking and molecular dynamics simulations demonstrate that calycosin stably binds to NLRP3 with high affinity, supporting its potential as an NLRP3 inhibitor. These findings indicate that calycosin protects against CIRI-induced BBB damage by inhibiting NLRP3-mediated pyroptosis and modulating tight junction protein expression, indicating that calycosin is a potential therapeutic option for ischemic stroke.

Mechanistically, PROX1 downregulates critical BBB-associated genes, including β-catenin and claudin-5, which are essential for BBB development and maintenance. These findings suggest that PROX1 compromises BBB integrity by negatively regulating BBB-associated gene expression and Wnt/β-catenin signaling.

We revealed glia-to-pericytes intercellular interactions and pericytic gene regulatory networks that are potentially perturbed by CAA and BBB breakdown. Future directions include analyzing external snRNAseq datasets and performing functional validations.

Presented results suggest that CLDNs may serve as biomarkers for diagnosis and prognosis as well as therapeutic targets in CNS tumors. Further investigation is essential to clarify their clinical relevance and therapeutic potential.