ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Annexin A3 Represses Endothelial Permeability and Inflammation During Sepsis via Actin Cytoskeleton Modulation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Gancao Nourishing-Yin decoction ameliorates endothelial inflammaging induced by serum from rheumatoid arthritis patients.Journal of traditional and complementary medicine · 2026Article
- Impact of altered HDL2b/HDL3 ratio on the function of innate immune cells in sepsis.Lipids in health and disease · 2026Article
- The macrophage DAG/PKCα/ROS axis exacerbates sepsis by inducing endothelial dysfunction through activation of the p38 MAPK pathway.Molecular biology reports · 2026Article
- Bioinformatics analysis of pyroptosis-related differentially expressed genes in sepsis and diabetes mellitus.PloS one · 2026Article
- Annexin A3 Represses Endothelial Permeability and Inflammation During Sepsis via Actin Cytoskeleton Modulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Interaction between endothelial injury and immune response in septic shock: from basic research to clinical applications.Frontiers in physiology · 2025Review
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5 authors.
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Abstract
Increased endothelial permeability and a dysregulated inflammatory response play key roles in organ damage in sepsis. The role of annexin A3 (ANXA3) in regulating endothelial permeability and inflammation during sepsis is explored using ANXA3 knockout mice and primary human umbilical vein endothelial cells (HUVECs). The absence of ANXA3 exacerbated sepsis outcomes, including increased mortality, lung injury, leukocyte infiltration, and vascular permeability. ANXA3 is highly expressed in endothelial cells and its loss results in the formation of cytoskeletal stress fibers and a decrease in the expression of the junction proteins zonula occludens (Zo)-1, vascular endothelial (VE)-cadherin, and claudin 5, leading to increase permeability. ANXA3 knockdown also upregulates E-selectin (CD62E) expression through the phosphorylation of activating transcription factor 2 (ATF2), which increases monocyte adhesion in HUVECs after LPS stimulation. Inhibiting actin polymerization reverse these effects. Thus, ANXA3 stabilizes the actin cytoskeleton, playing a protective role in endothelial dysfunction during sepsis.
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