Table 3.
Medications for treating sepsis and its complications by increasing HIF-1α expression
| Drug Names | The role of HIF-1α | Modulation of HIF-1α | Model | References |
|---|---|---|---|---|
| Rabeprazole | Facilitates vascular repair and resolution of lung injury | Up (directly HIF-1α pathway) | LPS-induced sepsis mouse | [36] |
| Roxadustat | Mitigates sepsis-induced acute lung injury | Up (PHD inhibitor) | I/R-induced AKI mouse mice | [37] |
| Acetate | Improved killing of S. pneumoniae by alveolar macrophages | Up (directly HIF-1α pathway) | S. pneumoniae infection mouse model | [109] |
| DMOG | Reducing Clostridium difficile toxin-induced intestinal damage | Up (PHD inhibitor) | Mouse ileal loop model | [74] |
| AKB-4924 | Enhances the cutaneous innate defenses against bacterial infections | Up (PHD inhibitor) | Mouse skin abscess model | [110] |
| Mimosine | Enhancement of the bactericidal capacity of phagocytes | Up (directly HIF-1α pathway) | S. aureus skin infection model | [111] |
| Edaravone | Exerts cardioprotective effects | Up (directlyHIF-1 α/HO-1 pathway) | CLP-induced sepsis rats | [112] |
| Phlorizin | Improve sepsis-induced cardiomyocyte injury | Up (induces the oxygen deprivation) | SIMD mouse model | [113] |
AKI acute kidney injury, CLP cecal ligation and puncture, DMOG Dimethyloxaloylglycine, HCP Houttuynia cordata polysaccharide, I/R ischemia/reperfusion, Ref. reference, S. aureus Staphylococcus aureus, S. pneumoniae Streptococcus pneumoniae, SIMD Sepsis-induced myocardial dysfunction