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Cell-cell junctions are essential for maintaining tissue integrity and regulating a wide range of physiological processes. While the disruption of intercellular junctions may lead to pathological conditions, it also presents an opportunity for therapeutic interventions. Nanomaterials have emerged as promising tools for modulating cell-cell junctions, offering new avenues for innovative treatments. In this review, we provide a comprehensive overview of the various nanomaterials interaction with cell-cell junctions. We discussed their underlying mechanisms, heterogenous effects on cellular behavior, and the therapeutic strategies of applying nanomaterial-induced intercellular junction disruption. Additionally, we address the challenges and opportunities involved in translating these strategies into clinical practice and discuss future directions for this rapidly advancing field.
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http://dx.doi.org/10.1016/j.cis.2024.103372 | DOI Listing |
ACS Nano
September 2025
Department of Emergency and Critical Care Medicine, The Fourth Affiliated Hospital of Soochow University, Suzhou 215124, China.
Acute lung injury (ALI) is characterized by the excessive accumulation of reactive oxygen species (ROS), which triggers a severe inflammatory cascade and the destruction of the alveolar-capillary barrier, leading to respiratory failure and life-threatening outcomes. Considering the limitations and adverse effects associated with current therapeutic interventions, developing effective and safe strategies that target the complex pathophysiological mechanisms of ALI is crucial for improving patient outcomes. Herein, we developed an inhalable, multifunctional nanotherapeutic (MSCNVs@CAT) by encapsulating catalase (CAT) in mesenchymal-stem-cell-derived nanovesicles (MSCNVs).
View Article and Find Full Text PDFbioRxiv
August 2025
Marine Eco-Evo-Devo Unit, Okinawa Institute of Science and Technology; Okinawa, 904-0495, Japan.
The diverse pigmentation patterns of animals are crucial for predation avoidance and behavioral display, yet mechanisms underlying this diversity remain poorly understood. In zebrafish, Turing models have been proposed to explain stripe patterns, but it is unclear if they apply to other fishes. In anemonefish (, we identified , a gene orthologous to zebrafish and encoding a connexin involved in pigment cell communication, as responsible for the phenotype.
View Article and Find Full Text PDFJ Cell Sci
September 2025
Department of Biochemistry, University of Illinois at Urbana-Champaign, IL, USA.
We present evidence that the association of Epithelial (E)-cadherin (CHD1) extracellular domain and epidermal growth factor receptor (EGFR, ErbB1) is obligatory for cadherin force transduction signaling. E-cadherin and EGFR associate at cell surfaces, independent of their cytoplasmic domains, and tension on E-cadherin activates EGFR signaling. Using engineered cadherin mutants that disrupt co-immunoprecipitation with EGFR, but not adhesion, we show that the hetero-receptor complex is required to mechanically activate signaling and downstream cytoskeletal remodeling at cadherin adhesions.
View Article and Find Full Text PDFCirc Res
September 2025
Department of Pediatrics, Child Health Research Center, University of Virginia School of Medicine, Charlottesville. (H.Y., M.Y., D.M., F.X., J.P.S., S.C., L.F.A., S.M., R.A.G., M.L.S.S.-L.).
Background: Juxtaglomerular cells are sensors that control blood pressure and fluid-electrolyte homeostasis. They are arranged as clusters at the tip of each afferent arteriole. In response to decreased blood pressure or extracellular fluid volume, juxtaglomerular cells secrete renin, initiating an enzymatic cascade that culminates in the production of Ang II (angiotensin II), a potent vasoconstrictor that restores blood pressure and fluid-electrolyte homeostasis.
View Article and Find Full Text PDFCommun Biol
September 2025
University of Münster, Institute of Integrative Cell Biology and Physiology, Münster, Germany.
The formation and maintenance of epithelia is critical for animal development and survival. Central to epithelial integrity are cadherin-based complexes called adherens junctions (AJs), which form physically robust but inherently dynamic cell-cell adhesions. How AJs function at the molecular level remains incompletely understood because techniques to study the central AJ proteins within the dynamic adhesion structure are scarce.
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