Table 2 Summary of candidate miRNA associated with sepsis

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]