Review Article

The Role of PPAR Gamma in Systemic Sclerosis

Table 2

In vivo studies of antifibrotic effects of PPARγ agonists.

Animal modelPPARγ ligandEffectsReference

Bleomycin-induced model of lung fibrosis15d-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]
RGZPrevented 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 fibrosisRGZAttenuated severity of dermal fibrosis and local collagen deposition
↓ Tissue accumulation of myofibroblasts
↓ Levels of TGF-β levels in lesional skin
[41]
Ajulemic acidPrevented 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 acidPrevented development of skin fibrosis
↓ Skin thickness dermal
↓ Hydroxyproline content
↓ Myofibroblasts number
[69]

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.