Table 1.
Mechanisms by which the WNT/β-catenin pathway is modulated and the possible roles of PPARγ agonists in treating SARS-CoV-2 infection.
| Target | Expression | Co-modulator | Disease complications | Model | References |
|---|---|---|---|---|---|
| WNT/β-catenin | Increase | TGF-β | Pulmonary fibrosis | COVID-19 patients | (65) |
| WNT/β-catenin | Increase | TGF-β | Pulmonary infection | COVID-19 patients | (10, 67) |
| serum IL-6 | Increase | – | – | COVID-19 patients | (72) |
| IL-10, TGF-β | Increase | PAI-1 | Pulmonary fibrosis | COVID-19 patients | (73) |
| TGF-β | Increase | – | ECM dysregulation | COVID-19 patients | (74, 75) |
| TGF-β | Increase | PAI-1 and collagen I | Lung fibrosis | SARS-coronavirus patients | (76) |
| ACE2 | Decrease | Spike (S) viral protein | Fibrosis, endothelial dysfunction, increased inflammation, oxidative stress | COVID-19 patients | (77–80) |
| ACE2 | Increase | pioglitazone | – | Animal models | (81) |
| ACE2 | Increase | pioglitazone | – | Hypothesis research in COVID-19 patients | (82) |
| NF-κB | Decrease | Pioglitazone | – | COVID-19 patients | (15, 83) |
| Cytokines storm | Decrease | PPARγ agonists | – | COVID-19 patients | (84–86) |
| SARS-CoV-2 RNA synthesis and replication | Decrease | Pioglitazone (as 3CL-Pro inhibitor) | – | Hypothesis research in COVID-19 patients | (87) |
ACE2, angiotensin-converting enzyme 2; COVID-19, Coronavirus disease 2019; Il-6, Interleukin-6; NF-κB, Nuclear factor-κB pathway; PPARγ, peroxisome proliferator-activated receptor gamma; SARS-CoV, severe acute respiratory syndrome coronavirus; TGF-β, transforming growth factor-beta; TNF-α, tumor necrosis factor-α.