Table 2.
Classic and novel therapeutic strategies directing to improvement of endothelial dysfunction in cirrhosis
| Therapeutic agent | Endothelial function | Ref. |
| Anti- inflammatory agents | Increase of NO bioavailability | [25,42,75,111] |
| Reduction of ADMA | ||
| Upregulation of eNOS activity | ||
| Decrease of Inflammation | ||
| Vitamins | Improvement of eNOS activity | [159,160,162] |
| Increase of NO bioavailability | ||
| Scavenging of ROS generation | ||
| Antioxidant function | ||
| Flavonoids | Increase of NO bioavailability | [15,166,168] |
| Prevention of oxidative stress | ||
| Improvement of antioxidant enzymes | ||
| Nuclear receptors | Increase of NO bioavailability | [33,50,187] |
| Improvement of DDAH | ||
| Reduction of ADMA | ||
| Amelioration of hepatic vascular tone | ||
| Ammonia lowering agents | Detoxification of ammonia levels | [27,189,190,192,201] |
| Increase of NO bioavailability | ||
| Reduction of ADMA | ||
| Upregulation DDAH expression | ||
| Statins | Decrease of total cholesterol | [147,170,172,202,203] |
| Improvement of Akt-dependent eNOS phosphorylation | ||
| Promoting NO biosynthesis | ||
| Reduction of Ox-LDL | ||
| Attenuation of inflammatory indices | ||
| Beta blockers | Amelioration of oxidative stress | [194,196] |
| Attenuation of Inflammation | ||
| Restoration of antioxidant enzymes | ||
| Angiotensin- receptor antagonists | Increase of NO | [200,204] |
| Decrease of Ang-II mediated inflammation | ||
| Decrease of TIMP-1, MMP-2 mediated fibrosis |
NO: Nitric oxide; ADMA: Asymmetric dimethylarginine; eNOS: Endothelial nitric oxide synthase; DDAH: Dimethyl arginine diaminohydrolase; Ox-LDL: Oxidized low-density lipoprotein; Ang II: Angiotensin II; TIMP-1: Tissue inhibitor of metalloproteinase 1; MMP-2: Matrix metalloproteinase-2.