ArticleShock (Augusta, Ga.)2018
Circulating Exosomes Isolated from Septic Mice Induce Cardiovascular Hyperpermeability Through Promoting Podosome Cluster Formation.
Article in Shock (Augusta, Ga.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Mitochondria-Derived Vesicles and Mitochondrial Extracellular Vesicles in Health and Cardiovascular Disease.Circulation research · 2026Review
- Roles and Therapeutic Targeting of Exosomes in Sepsis-Induced Cardiomyopathy.Journal of cellular and molecular medicine · 2025Review
- Pathogenic and therapeutic roles of extracellular vesicles in sepsis.Frontiers in immunology · 2025Review
- Exosomes as novel biomarkers in sepsis and sepsis related organ failure.Journal of translational medicine · 2024Review
- Macrophages in sepsis-induced acute lung injury: exosomal modulation and therapeutic potential.Frontiers in immunology · 2024Review
- Unraveling the Intricate Roles of Exosomes in Cardiovascular Diseases: A Comprehensive Review of Physiological Significance and Pathological Implications.International journal of molecular sciences · 2023Review
- Lipocalin 10 is essential for protection against inflammation-triggered vascular leakage by activating LDL receptor-related protein 2-slingshot homologue 1 signalling pathway.Cardiovascular research · 2023Article
- A bibliometric analysis of sepsis-induced myocardial dysfunction from 2002 to 2022.Frontiers in cardiovascular medicine · 2023Article
- Article
- Extracellular vesicles participate in the pathogenesis of sepsis.Frontiers in cellular and infection microbiology · 2022Review
- Cellular and Exosomal Regulations of Sepsis-Induced Metabolic Alterations.International journal of molecular sciences · 2021Review
- Therapeutic Potential of Extracellular Vesicles for Sepsis Treatment.Advanced therapeutics · 2021Article
- Sectm1a Facilitates Protection against Inflammation-Induced Organ Damage through Promoting TRM Self-Renewal.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Dark-Side of Exosomes.Advances in experimental medicine and biology · 2021Article
- Intestinal Epithelium-Derived Luminally Released Extracellular Vesicles in Sepsis Exhibit the Ability to Suppress TNF-a and IL-17A Expression in Mucosal Inflammation.International journal of molecular sciences · 2020Article
- Identification of a Novel Antisepsis Pathway: Sectm1a Enhances Macrophage Phagocytosis of Bacteria through Activating GITR.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- The Art of Intercellular Wireless Communications: Exosomes in Heart Disease and Therapy.Frontiers in cell and developmental biology · 2019Review
- Extracellular Vesicles as Markers and Mediators in Sepsis.Theranostics · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Septic shock increases vascular permeability, leading to multiple organ failure including cardiac dysfunction, a major contributor to septic death. Podosome, an actin-based dynamic membrane structure, plays critical roles in extracellular matrix degradation and angiogenesis. However, whether podosome contributes to endothelial barrier dysfunction during septic shock remains unknown. In this study, we found that the endothelial hyperpermeability, stimulated by phorbol 12-myristate 13-acetate and thrombin, was accompanied by increased formation of podosome clusters at the cell periphery, indicating a positive correlation between podosome clusters and endothelial leakage. Interestingly, we observed that circulating exosomes collected from septic mice were able to stimulate podosome cluster formation in cardiac endothelial cells, together with increased permeability in vitro/in vivo and cardiac dysfunction. Mechanistically, we identified that septic exosomes contained higher levels of reactive oxygen species (ROS) than normal ones, which were effectively transported to endothelial cells (ECs). Depletion of ROS in septic exosomes significantly reduced their capacity for promoting podosome cluster formation and thereby dampened vascular leakage. Finally, we elucidated that podosome cluster-induced endothelial hyperpermeability was associated with fragmentation/depletion of zonula occludens-1 (ZO-1) at the cell periphery. Our results demonstrate that septic exosomes were enriched with high amounts of ROS, which can be transported to ECs, leading to the generation of podosome clusters in target ECs and thereby, causing ZO-1 relocation, vascular leakage, and cardiac dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.