Table 1.
Selected lncRNAs Involved in Sepsis
| lncRNAs | Expression in Sepsis | Target Gene | Effect(s) | Model | No. of Samples | Ref. |
|---|---|---|---|---|---|---|
| MALAT1 | up | miR-125b | MALAT1 interacts with p38 MAPK/NF-κB and miR-125b, thereby aggravating cardiac inflammation and dysfunction in sepsis | mice | – | 216 |
| NEAT1 | up | miR-204 | the upregulation of NEAT1 was related to the severity of acute kidney injury (AKI) in sepsis patients | humans in vitro | 55 | 217 |
| NEAT1 | up | circulating lncRNA NEAT1 was related to severity, increased risk, and unfavorable prognosis in sepsis patients | humans | 152 | 218 | |
| NEAT1 | up | NEAT1 induced brain injury in septic mice via positively regulating NF-κB | Mice | – | 219 | |
| NEAT1 | up | – | – | humans | 59 | 220 |
| lnc-ANRIL | up | – | – | humans | 26 | 221 |
| lnc-ANRIL/miR-125a axis | up | lnc-ANRIL/miR-125a axis could serve as a biomarker for prognosis, severity, and inflammation in sepsis patients | humans | 26 | 221 | |
| HOTAIR | up | HOTAIR upregulation leads to HK-2 cell apoptosis in kidney injury via the miR-22/HMGB1 pathway | rats in vitro | – | 222 | |
| HOTAIR | – | HOTAIR overexpression can reduce AKI in septic rats by suppressing the apoptosis of kidney tissues via downregulating the miR-34a/Bcl-2 signaling pathway | Rats | – | 223 | |
| lncRNA H19 | down | – | humans in vitro | 69 | 224 | |
| lncRNA ITSN1-2 | up | high expression of ITSN1-2 is associated with disease severity and inflammation in sepsis patients. | Humans | 309 | 225 | |
| HULC | up | – | upregulation of lncRNA HULC is required for the pro-inflammatory response during LPS induced sepsis. | mice in vitro | – | 226 |
| UCA1 | upregulation of UCA1 is needed for the response of pro-inflammatory immune cells during LPS-induced sepsis | |||||
| TUG1 | down | decreased TUG1 expression may induce sepsis-related AKI by modulating the NF-κB pathway and regulating the miR-142-3p/SIRT1 axis | humans in vitro | 28 | 227 | |
| TapSAKI | up | TapSAKI promoted the inflammatory response and HK-2 cell apoptosis through the miR-22/PTEN/TLR4/NF-κB pathway | rats in vitro | – | 228 | |
| HOTAIR | up | - | in vivo studies showed that silencing of HOTAIR could improve cardiac function of septic mice and significantly reduce TNF-α production | Mice | 14 | |
| MALAT1 | up | – | IL-6 induced upregulation of MALAT1 in LPS-treated cardiomyocytes, and MALAT1 could promote the expression of TNF-α at least partly by SAA3 in response to LPS treatment in cardiomyocytes | mice in vitro | – | 229 |
| MALAT1 and EZH2 | up | – | upregulation of MALAT1 and EZH2 were found in the hearts of rats with sepsis | rats in vitro | – | 230 |