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@ARTICLE{Dragomir:277773,
      author       = {M.-P. Dragomir$^*$ and E. Fuentes-Mattei and M. Winkle and
                      K. Okubo and R. Bayraktar and E. Knutsen and A. Qdaisat and
                      M. Chen and Y. Li and M. Shimizu and L. Pang and K. Liu and
                      X. Liu and S. Anfossi and H. Zhang and I. Koch and A. M.
                      Tran and S. Mohapatra and A. Ton and M. Kaplan and M. W.
                      Anderson and S. J. Rothfuss and R. Silasi and R. S. Keshari
                      and M. Ferracin and C. Ivan and C. Rodriguez-Aguayo and G.
                      Lopez-Berestein and C. Georgescu and P. P. Banerjee and R.
                      Basar and Z. Li and D. Horst$^*$ and C. Vasilescu and M. T.
                      S. Bertilaccio and K. Rezvani and F. Lupu and S.-C. Yeung
                      and G. A. Calin},
      title        = {{A}nti-mi{R}-93-5p therapy prolongs sepsis survival by
                      restoring the peripheral immune response.},
      journal      = {The journal of clinical investigation},
      volume       = {133},
      number       = {14},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2023-01488},
      pages        = {e158348},
      year         = {2023},
      abstract     = {Sepsis remains a leading cause of death for humans and
                      currently has no pathogenesis-specific therapy. Hampered
                      progress is partly due to a lack of insight into deep
                      mechanistic processes. In the past decade, deciphering the
                      functions of small noncoding miRNAs in sepsis pathogenesis
                      became a dynamic research topic. To screen for new miRNA
                      targets for sepsis therapeutics, we used samples for miRNA
                      array analysis of PBMCs from patients with sepsis and
                      control individuals, blood samples from 2 cohorts of
                      patients with sepsis, and multiple animal models: mouse
                      cecum ligation puncture-induced (CLP-induced) sepsis, mouse
                      viral miRNA challenge, and baboon Gram+ and Gram- sepsis
                      models. miR-93-5p met the criteria for a therapeutic target,
                      as it was overexpressed in baboons that died early after
                      induction of sepsis, was downregulated in patients who
                      survived after sepsis, and correlated with negative clinical
                      prognosticators for sepsis. Therapeutically, inhibition of
                      miR-93-5p prolonged the overall survival of mice with
                      CLP-induced sepsis, with a stronger effect in older mice.
                      Mechanistically, anti-miR-93-5p therapy reduced inflammatory
                      monocytes and increased circulating effector memory T cells,
                      especially the CD4+ subset. AGO2 IP in miR-93-KO T cells
                      identified important regulatory receptors, such as CD28, as
                      direct miR-93-5p target genes. In conclusion, miR-93-5p is a
                      potential therapeutic target in sepsis through the
                      regulation of both innate and adaptive immunity, with
                      possibly a greater benefit for elderly patients than for
                      young patients.},
      keywords     = {Humans / Mice / Animals / Aged / Antagomirs / MicroRNAs:
                      genetics / Adaptive Immunity / Sepsis: pathology / Adaptive
                      immunity (Other) / Immunology (Other) / Infectious disease
                      (Other) / Innate immunity (Other) / Noncoding RNAs (Other) /
                      Antagomirs (NLM Chemicals) / MicroRNAs (NLM Chemicals) /
                      MIRN93 microRNA, human (NLM Chemicals)},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37261908},
      pmc          = {pmc:PMC10348769},
      doi          = {10.1172/JCI158348},
      url          = {https://inrepo02.dkfz.de/record/277773},
}