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Pathological condition | PPAR isotype/ligand | Ligand-induced effects | Affected signaling pathway | Reference |
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Endotoxic shock | PPARα/fenofibrate | Decrease in coagulation activation (monocyte tissue factor expression), protection against endothelial dysfunction | Not examined | Wiel et al. [107] |
PPARγ/rosiglitazone | Suppression of biomarkers for liver and kidney injury and of cytokines, inhibition of heart rate increase | Not examined | Wu et al. [110] |
PPARγ/15d-PGJ2 | Improvement of survival rate, reduction of adhesion molecule expression, and of neutrophil infiltration in tissues | NF-κB, HSP (heat shock protein) 70 | Kaplan et al. [104] |
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Hemorrhagic shock | PPARγ/ciglitazone | Amelioration of mean arterial pressure, reduction of plasma cytokine levels, decrease of apoptosis in lung and liver | NF-κB | Chima et al. [112] |
Caspase-3, PI3/Akt | Chima et al. [113], Zingarelli et al. [105] |
PPARγ/15d-PGJ2 | Attenuation of renal dysfunction and of liver, lung, and intestine injury | Not examined | Abdelrahman et al. [111] |
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Polymicrobial sepsis/septic shock | PPARβ/δ | Decrease in cytokine release, attenuation of organ dysfunction, reduced expression of inducible nitric oxide synthase | Akt, GSK-3β, ERK1/2, STAT-3, NF-κB | Kapoor et al. [106] |
Zingarelli et al. [115] |
PPARγ/ciglitazone and 15d-PGJ2 | Amelioration of hypotension and survival, decreased inflammatory signs in lung, colon, and liver | NF-κB, AP-1 | Zingarelli et al. [114] |
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Multiple organ failure | PPARβ/δ | Reduction of peritoneal exsudate formation and of neutrophil infiltration, attenuation of multiple organ dysfunction syndrome | Not examined | Galuppo et al. [117] |
PPARγ/rosiglitazone | Attenuation of peritoneal exsudation and of organ injury and dysfunction | Not examined | Cuzzocrea et al. [116] |
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