Hepatic ischemia-reperfusion syndrome and its effect on the cardiovascular system: The role of treprostinil, a synthetic prostacyclin analog

Table 2 Treprostinil mechanisms of action

Effect	Mechanism of action	Cellular response
Vessel tone	cAMP increased. Endothelin 1 decreased. Potassium decreased	Vasodilation. Improvement of microcirculation dysfunction
Antiproliferative	PPARs increased. cAMP increased. VEGF-A increased	Angiogenesis. Regulation of vascular homeostasis
Antithrombotic	Thromboxane A2 decreased. PDGF decreased	Inhibition of platelets aggregation. Platelets adherence decreased
Anti-inflammatory	P38 and JNK cascades decreased. IL-1, IL-6, TNF-α decreased. IL-10 increased. Reactive oxygen species decreased. TLR 9 decreased	Attenuation of inflammatory cascade. Apoptosis rate increased
Energy balance	Pgc-1α mRNA expression decreased. Cytochrome c decreased. Caspase 3 activation decreased	ATP production increased. Mitochondrial biogenesis increased

cAMP: Cyclic adenosine monophosphate; PPARs: Peroxisome proliferator-activated receptors; VEGF: Vascular endothelial-derived growth factor; JNK: c-Jun N-terminal kinase; IL: Interleukin; TNF: Tumor necrosis factor; TLR: Toll-like-receptor; ATP: Adenosine triphosphate.