Exosomes in Sepsis and Inflammatory Tissue Injury.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Additional Information
    • Source:
      Publisher: Bentham Science Publishers Country of Publication: United Arab Emirates NLM ID: 9602487 Publication Model: Print Cited Medium: Internet ISSN: 1873-4286 (Electronic) Linking ISSN: 13816128 NLM ISO Abbreviation: Curr Pharm Des Subsets: MEDLINE
    • Publication Information:
      Publication: Saif Zone, Sharjah, U.A.E. : Bentham Science Publishers
      Original Publication: Schiphol, The Netherlands : Bentham Science Publishers, c1995-
    • Subject Terms:
      Exosomes/*physiology ; Inflammation/*pathology ; Sepsis/*pathology; Cytokines ; Humans ; Multiple Organ Failure
    • Abstract:
      Sepsis is the leading cause of death in medical intensive care units, and thus represents a serious healthcare problem worldwide. Sepsis is often caused by the aberrant host responses to infection, which induce dysregulated inflammation that leads to life-threatening multiple organ failures. Mediators such as proinflammatory cytokines that drive the sepsis pathogenesis have been extensively studied. Exosomes, biological lipid bilayer nanoparticles secreted via the endosomal pathway of cells, have recently emerged as important cargos that carry multiple mediators critical for the pathogenesis of sepsis-associated organ dysfunctions. Here we will review current knowledge on the exosomes in sepsis and relevant inflammatory tissue injuries.
      (Copyright© Bentham Science Publishers; For any queries, please email at [email protected].)
    • Contributed Indexing:
      Keywords: Sepsis; exosome; extracellular vesicle; inflammatory tissue injury; integrin; miRNA; septic shock.
    • Accession Number:
      0 (Cytokines)
    • Publication Date:
      Date Created: 20191119 Date Completed: 20200617 Latest Revision: 20200617
    • Publication Date:
      20240829
    • Accession Number:
      10.2174/1381612825666191116125525
    • Accession Number:
      31738129