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The tight junction (TJ), a type of cell-cell junction, regulates the permeability of solutes across epithelial and endothelial cellular sheets and is believed to maintain cell polarity. However, recent studies have provided conflicting views on the roles of TJs in epithelial polarity. Membrane proteins, including occludin, claudin, and the junction adhesion molecule, have been identified as TJ components. TJs are predominantly found at the stratum granulosum and stratum corneum. Although it remains unclear whether the disruption of TJs is the cause or consequence of certain dental diseases, evidence suggests that TJ dysfunction may be a crucial factor in gingival epithelial barrier impairment and the progression of oral diseases. Bacterial infection is among the most specific factors we found that may contribute to the breakdown of the epithelial barrier formed by TJs in dental diseases. Bacteria and their products may weaken the epithelial barrier by directly destroying intercellular junctions or altering the expression of junctional proteins. Additionally, they may induce the production of inflammatory cytokines, which could lead to the downregulation of TJ proteins and, consequently, impair the epithelial barrier. This review introduces a novel perspective by exploring, for the first time, the role of TJs dysfunction in the breakdown of the oral epithelial barrier and its potential link to the progression of dental diseases such as gingivitis, periodontitis, Sjӧgren syndrome, and oral squamous cell carcinoma.
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http://dx.doi.org/10.2147/CCIDE.S492107 | DOI Listing |
Biomed J
September 2025
Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University. Electronic address:
Background: Lung cancer is the leading cause of cancer-related mortality worldwide. Although immune checkpoint inhibitors (ICIs), chemotherapy, and molecular targeted therapies have improved survival rates, therapeutic resistance remains a major barrier to curative outcomes. Recently, plasminogen activator inhibitor-1 (PAI-1) has been implicated in lung cancer progression and treatment resistance.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
School of Pharmacy, Shanghai Jiao Tong University, Shanghai, 200240, PR China. Electronic address:
Ulcerative colitis (UC), a chronic inflammatory bowel disease (IBD), is characterized by disruption of intestinal barrier function and complex inflammatory manifestations locally and systemically. Although anti-tumor necrosis factor-α (TNF-α) agents such as Infliximab (IFX) are effective in treating IBD, their intestinal tissue concentration has been regarded as determinant of therapeutic efficacy while was restrained by the large molecular weight. Considering the enhanced expression of human neonatal Fc receptor (hFcRn) in UC tissues, we attempted to deliver the therapeutic entity of IFX into UC tissues by developing a novel dual-acting IFX Fab-F8 (IFX-F8) fusion protein for UC treatment.
View Article and Find Full Text PDFAdv Drug Deliv Rev
September 2025
J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, United States; Emerging Pathogens Institute, University of Florida, Gainesville, FL, United States. Electronic address:
The human microbiome plays a critical role in health and disease. Disruptions in microbiota composition or function have been implicated not only as markers but also as drivers of diverse pathologies, creating opportunities for targeted microbiome interventions. Advancing these therapies requires experimental models that can unravel the complex, bidirectional interactions between human tissue and microbial communities.
View Article and Find Full Text PDFJ Control Release
September 2025
Department of Pharmaceutics, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou City, Zhejiang Province 325035, China. Electronic address:
Gut barrier loss exacerbated gut microbiota dysbiosis by permitting pathogenic blooms, while gut microbiota dysbiosis caused the development of gut mucosal wounds by reducing mucus and breaking down epithelial tight junction. Current therapies combating colitis often fail to address both gut barrier dysfunction and microbial imbalance. Herein, inspired by natural gut mucus, a dual-crosslinked hydrogel (HSMP-LA) composed of thiol/maleimide-modified hyaluronic acid together with co-loading of antimicrobial ε-polylysine (ε-PL) and larazotide acetate (LA) had been developed as an injectable artificial gut mucus to simultaneously restore barrier integrity and modulate gut microbiota.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Clinical Pharmacy Department, School of Pharmacy, Newgiza University, Giza, Egypt. Electronic address:
Ulcerative colitis (UC) is a persistent inflammatory condition marked by the destruction of the intestinal mucosal barrier, infiltration of inflammatory cells, and ulceration. M1/M2 macrophage polarization plays an imperative function in the regulation of inflammation through the nuclear factor-kappa B (NFκB) signaling pathway and modulating microRNA-155 (miR-155). Recent studies have highlighted the anti-ulcerogenic and colo-protective properties of sodium-glucose co-transporter-2 (SGLT2) inhibitors.
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