Endothelial dysfunction in cirrhosis: Role of inflammation and oxidative stress

Table 1 Factors affecting endothelial dysfunction in cirrhosis

Marker	Endothelial dysfunction	Ref.
Inflammatory marker
TNF-α	Inhibition of NO synthesis	[47,75,78,84,99,104]
NFκB	Increase of ADMA
TLR	Increase of Caveolin-1
Ang II	Reduction of eNOS activity
	Inhibition of DDAH enzyme
	Upregulation of iNOS
	Increase of superoxide production
	Reduction of antioxidant capacity
Oxidative marker
4-HNE	Reduction of DDAH enzyme activity	[42,78,104]
NADPH	Decrease of NO bioavailability
	Increase of ADMA levels
	Increase of ROS generation
Cyclooxygenase -derived prostanoids
TXA2	Reduction of intrahepatic nitrate/nitrite	[110-112]
PGI2	Upregulation of iNOS expression
	Increase of intrahepatic resistance
Other marker
ET-1	Increase of inflammation	[122,130,138,139, 145]
LOX-1	Stimulation of ROS generation
PARs
Adiponectin
Palmitic acid

TNF-α: Tumor necrosis factor-α; NFκB; Nuclear factor kappa B; TLR: Toll like receptor; Ang II: Angiotensin II; NO: Nitric oxide; ADMA: Asymmetric dimethylarginine; eNOS: Endothelial nitric oxide synthase; DDAH: Dimethyl arginine diaminohydrolase; iNOS: Inducible nitric oxide synthase; 4-HNE: 4-hydroxy-2-nonenal; NADPH; Nicotinamide adenine dinucleotide phosphate-oxidase; ROS: Reactive oxygen species; TXA2: Thromboxane A2; PGI2: Prostaglandin I2; ET-1: Endothelin -1; LOX-1: Lectin-like oxidized low-density lipoprotein receptor-1; PARs: Protease activated receptors.