Article: Emerging Therapeutic Targets for Portal Hypertension.
2023 Volume 22, Issue 1, Page(s) 51–66
Abstract: Purpose of review: Portal hypertension is responsible of the main complications of cirrhosis, which carries a high mortality. Recent treatments have improved prognosis, but this is still far from ideal. This paper reviews new potential therapeutic ... ...
Abstract | Purpose of review: Portal hypertension is responsible of the main complications of cirrhosis, which carries a high mortality. Recent treatments have improved prognosis, but this is still far from ideal. This paper reviews new potential therapeutic targets unveiled by advances of key pathophysiologic processes. Recent findings: Recent research highlighted the importance of suppressing etiologic factors and a safe lifestyle and outlined new mechanisms modulating portal pressure. These include intrahepatic abnormalities linked to inflammation, fibrogenesis, vascular occlusion, parenchymal extinction, and angiogenesis; impaired regeneration; increased hepatic vascular tone due to sinusoidal endothelial dysfunction with insufficient NO availability; and paracrine liver cell crosstalk. Moreover, pathways such as the gut-liver axis modulate splanchnic vasodilatation and systemic inflammation, exacerbate liver fibrosis, and are being targeted by therapy. We have summarized studies of new agents addressing these targets. Summary: New agents, alone or in combination, allow acting in complementary mechanisms offering a more profound effect on portal hypertension while simultaneously limiting disease progression and favoring regression of fibrosis and of cirrhosis. Major changes in treatment paradigms are anticipated. |
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Language | English |
Publishing date | 2023-02-11 |
Publishing country | United States |
Document type | Journal Article ; Review |
ZDB-ID | 2813071-6 |
ISSN | 2195-9595 ; 2195-9595 ; 1540-3416 |
ISSN (online) | 2195-9595 |
ISSN | 2195-9595 ; 1540-3416 |
DOI | 10.1007/s11901-023-00598-4 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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