Review Article
The Role of PPAR Gamma in Systemic Sclerosis
Table 2
In vivo studies of antifibrotic effects of PPARγ agonists.
| Animal model | PPARγ ligand | Effects | Reference |
| Bleomycin-induced model of lung fibrosis | 15d-PGJ2 and RGZ | ↓ Histological evidence of lung fibrosis | [61] | TGZ | ↓ Hydroxyproline and collagen deposition in lung tissue Ameliorated histopathological changes | [47] | PGZ | ↓ Hydroxyproline content in lung tissue Ameliorated histopathological changes | [60] | RGZ | Prevented onset of fibrotic radiological changes | [63] | RGZ | ↓ Hydroxyproline content in lung tissue ↓ Lung TGF-β1 concentration Ameliorated histopathological changes | [62] |
| Bleomycin-induced model of skin fibrosis | RGZ | Attenuated severity of dermal fibrosis and local collagen deposition ↓ Tissue accumulation of myofibroblasts ↓ Levels of TGF-β levels in lesional skin | [41] | Ajulemic acid | Prevented development of skin fibrosis ↓ Skin thickness dermal ↓ Hydroxyproline content ↓ Myofibroblasts number | [69] | CDDO | ↓ Collagen deposition and dermal thickness ↓ α-SMA and TGFβ1 expression | [27] |
| Constitutively active TGFβ receptor type I mouse model (AdTGFbRI) | Ajulemic acid | Prevented development of skin fibrosis ↓ Skin thickness dermal ↓ Hydroxyproline content ↓ Myofibroblasts number | [69] |
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RGZ = rosiglitazone, TGZ = troglitazone, PGZ = pioglitazone, CDDO = 2-cyano-3,12-dioxoolean-1,9-dien-28-oic-acid, TGF-β = transforming growth factor-β, α-SMA = α-smooth muscle actin.
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