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Table 2 Summary of candidate miRNA associated with sepsis

From: Plasma levels of microRNA are altered with the development of shock in human sepsis: an observational study

miRNA Findings
miR-15a Differentially expressed in adult and neonatal sepsis [18, 19]. Inhibits angiogenesis through direct targeting of VEGF and FGF [51]
miR-16 Differentially expressed in adult and neonatal sepsis [18, 19]. Regulates cell cycle entry, differentiation, and cytokine production in EPCs [52]
miR-34a Plasma expression altered in murine sepsis [14]. Promotes endothelial senescence through targeting of SIRT1 [53]
miR-126 Plasma expression altered in murine sepsis [14]. Regulates the response of endothelial cells to VEGF through targeting of SPRED1 [15]
miR-27a Upregulated in the lungs of septic mice [20, 21]. Knockdown reduced levels of TNF-α and IL-6 [21]
miR-150 Elevated in septic patients compared to patients with nonseptic SIRS [23]
Lower levels of miR-150 associated with sepsis mortality [22]
miR-223 Elevated in septic patients compared to controls
Expression level directly related to illness severity [25]
miR-181b Inhibits NF-κB-mediated expression of VCAM1 in endothelial cells and reduces leukocyte influx into vascular endothelium [26]
miR-155 Upregulated in mice in response to systemic lipopolysaccharide. Targets several proteins in LPS signaling pathway [27]
miR-125b Downregulated in mice in response to systemic lipopolysaccharide. Targets TNF-α [27]
miR-146a Regulates IL-1β, IL-6, and TNF-α expression through targeting of IRAK1 in the NF-κB signaling pathway [28]
miR-486 Targets and inhibits NF-κB repressors resulting in its sustained signaling [29]
miR-21 Upregulated in mice in response to cecal ligation and puncture. Shown to facilitate the generation of myeloid-derived suppressor cells in late sepsis [30] Null miR-21 mice with higher mortality in LPS-peritonitis model [31]
  1. miRNA microRNA, VEGF vascular endothelial growth factor, FGF fibroblast growth factor, EPC endothelial progenitor cells, TNF-α tumor necrosis factor alpha, IL-6 interleukin-6, SIRS systemic inflammatory response syndrome, NF-κB nuclear factor kappa B, LPS lipopolysaccharide, IL-1β interleukin-1 beta