Table 1.

Selected publications on experimental studies testing the anti-inflammatory effects of PPAR ligands in various models of sepsis and shock.

Pathological condition	PPAR isotype/ligand	Ligand-induced effects	Affected signaling pathway	Reference
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]
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]
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]
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]