Table 1.
Manipulation | Upstream of FoxO1 | FoxO1 activity | Effect on macrophage | Disease phenotype | Reference |
---|---|---|---|---|---|
Chemical compounds | |||||
AS1842856 | — | Inhibited | M2↓ | Asthma↓ | [36] |
Ang- [1–7] | TLR4–JNK | Inhibited | M1↓ | Inflammation ↓ | [47] |
AA | JNK | Inhibited | Proliferation↓ | — | [48] |
ATRA | RARα | Inhibited | M2↑ | Liver ischemia -reperfusion injury↓ | [49] |
ICG-001 | β-Catenin | Enhanced | MMT↓ | Kidney fibrosis↓ | [21] |
Genetic (indirect) | |||||
Nrf2 cKO | Nrf2–Akt | Inhibited | M1↑ | Liver ischemia -reperfusion injury↑ | [50] |
CypD cKO | — | Inhibited | M1↓ | Inflammation ↓ | [37] |
LysM-Irs2 | Akt | M2↓ | Obesity↑ | [18] | |
LysM-Sirt6 | — | Enhanced | M1↑ | Rheumatoid arthritis↑ | [20] |
LysM-PTEN | — | Inhibited | M1↓ | Acute lung injury ↓ | [43] |
PTEN siRNA | Akt/β-catenin | Inhibited | M1↓ | Liver ischemia -reperfusion injury↓ | [51] |
CaMKKβ siRNA | — | Enhanced | Autophagy↑ | Anti-bacteria↑ | [22] |
LKB1 vector | — | Enhanced | M1↑ | Tuberculosis infection↓ | [16] |
ADAR1 adenovirus | miR-21 | Enhanced | M2↑ | Allogeneic graft rejection↓ | [34] |
Genetic (direct) | |||||
LysM-FoxO1 | — | Inhibited | M2↑; M1↓ | S. aureus infection↑ | [23] |
LysM-FoxO1 | HIF-1α | Inhibited | M2↑ | Tumor↑ | [32] |
FoxO1 cKO | TLR4-PI3K-Akt | Inhibited | M1↓ | Obesity↓ | [17] |
FoxO1 shRNA | Insulin–Akt | Inhibited | Apoptosis↓ | Obesity↓ | [1] |
Abbreviations: AS1842856, a pharmacologic inhibition of FoxO1; Ang, angiotensin; AA, arachidonic acid; ATRA, all-trans retinoic acid; RARα, retinoic acid receptor α; ICG-001,a known inhibitor of β-catenin/TCF transcription by selectively blocking the β-catenin/CREB-binding protein interaction; MMT, macrophage–myofibroblast transition; Nrf2, nuclear factor erythroid 2-related factor 2; CypD, cyclophilin D; PTEN, phosphatase and tensin homologue; LKB1, liver kinase B1; ADAR1, adenosine deaminase acting on double-stranded RNA 1.