Emerging Therapeutic Targets for Portal Hypertension

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...
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Autor*in:	Felli, Eric [verfasserIn] Nulan, Yelidousi Selicean, Sonia Wang, Cong Gracia-Sancho, Jordi Bosch, Jaume

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Portal hypertension Cirrhosis of the liver Fibrosis Endothelial dysfunction Hepatic vascular resistance

Anmerkung:	© The Author(s) 2023

Übergeordnetes Werk:	Enthalten in: Current hepatitis reports - Philadelphia, Pa : Current Science Inc., 2002, 22(2023), 1 vom: 11. Feb., Seite 51-66
Übergeordnetes Werk:	volume:22 ; year:2023 ; number:1 ; day:11 ; month:02 ; pages:51-66

Links:	Volltext

DOI / URN:	10.1007/s11901-023-00598-4

Katalog-ID:	SPR049564188

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allfields	10.1007/s11901-023-00598-4 doi (DE-627)SPR049564188 (SPR)s11901-023-00598-4-e DE-627 ger DE-627 rakwb eng Felli, Eric verfasserin (orcid)0000-0002-5664-6746 aut Emerging Therapeutic Targets for Portal Hypertension 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 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. Portal hypertension (dpeaa)DE-He213 Cirrhosis of the liver (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Endothelial dysfunction (dpeaa)DE-He213 Hepatic vascular resistance (dpeaa)DE-He213 Nulan, Yelidousi aut Selicean, Sonia aut Wang, Cong aut Gracia-Sancho, Jordi aut Bosch, Jaume (orcid)0000-0003-3414-0055 aut Enthalten in Current hepatitis reports Philadelphia, Pa : Current Science Inc., 2002 22(2023), 1 vom: 11. Feb., Seite 51-66 (DE-627)357168275 (DE-600)2094164-X 1541-0706 nnns volume:22 year:2023 number:1 day:11 month:02 pages:51-66 https://dx.doi.org/10.1007/s11901-023-00598-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 AR 22 2023 1 11 02 51-66
spelling	10.1007/s11901-023-00598-4 doi (DE-627)SPR049564188 (SPR)s11901-023-00598-4-e DE-627 ger DE-627 rakwb eng Felli, Eric verfasserin (orcid)0000-0002-5664-6746 aut Emerging Therapeutic Targets for Portal Hypertension 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 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. Portal hypertension (dpeaa)DE-He213 Cirrhosis of the liver (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Endothelial dysfunction (dpeaa)DE-He213 Hepatic vascular resistance (dpeaa)DE-He213 Nulan, Yelidousi aut Selicean, Sonia aut Wang, Cong aut Gracia-Sancho, Jordi aut Bosch, Jaume (orcid)0000-0003-3414-0055 aut Enthalten in Current hepatitis reports Philadelphia, Pa : Current Science Inc., 2002 22(2023), 1 vom: 11. Feb., Seite 51-66 (DE-627)357168275 (DE-600)2094164-X 1541-0706 nnns volume:22 year:2023 number:1 day:11 month:02 pages:51-66 https://dx.doi.org/10.1007/s11901-023-00598-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 AR 22 2023 1 11 02 51-66
allfields_unstemmed	10.1007/s11901-023-00598-4 doi (DE-627)SPR049564188 (SPR)s11901-023-00598-4-e DE-627 ger DE-627 rakwb eng Felli, Eric verfasserin (orcid)0000-0002-5664-6746 aut Emerging Therapeutic Targets for Portal Hypertension 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 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. Portal hypertension (dpeaa)DE-He213 Cirrhosis of the liver (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Endothelial dysfunction (dpeaa)DE-He213 Hepatic vascular resistance (dpeaa)DE-He213 Nulan, Yelidousi aut Selicean, Sonia aut Wang, Cong aut Gracia-Sancho, Jordi aut Bosch, Jaume (orcid)0000-0003-3414-0055 aut Enthalten in Current hepatitis reports Philadelphia, Pa : Current Science Inc., 2002 22(2023), 1 vom: 11. Feb., Seite 51-66 (DE-627)357168275 (DE-600)2094164-X 1541-0706 nnns volume:22 year:2023 number:1 day:11 month:02 pages:51-66 https://dx.doi.org/10.1007/s11901-023-00598-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 AR 22 2023 1 11 02 51-66
allfieldsGer	10.1007/s11901-023-00598-4 doi (DE-627)SPR049564188 (SPR)s11901-023-00598-4-e DE-627 ger DE-627 rakwb eng Felli, Eric verfasserin (orcid)0000-0002-5664-6746 aut Emerging Therapeutic Targets for Portal Hypertension 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 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. Portal hypertension (dpeaa)DE-He213 Cirrhosis of the liver (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Endothelial dysfunction (dpeaa)DE-He213 Hepatic vascular resistance (dpeaa)DE-He213 Nulan, Yelidousi aut Selicean, Sonia aut Wang, Cong aut Gracia-Sancho, Jordi aut Bosch, Jaume (orcid)0000-0003-3414-0055 aut Enthalten in Current hepatitis reports Philadelphia, Pa : Current Science Inc., 2002 22(2023), 1 vom: 11. Feb., Seite 51-66 (DE-627)357168275 (DE-600)2094164-X 1541-0706 nnns volume:22 year:2023 number:1 day:11 month:02 pages:51-66 https://dx.doi.org/10.1007/s11901-023-00598-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 AR 22 2023 1 11 02 51-66
allfieldsSound	10.1007/s11901-023-00598-4 doi (DE-627)SPR049564188 (SPR)s11901-023-00598-4-e DE-627 ger DE-627 rakwb eng Felli, Eric verfasserin (orcid)0000-0002-5664-6746 aut Emerging Therapeutic Targets for Portal Hypertension 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 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. Portal hypertension (dpeaa)DE-He213 Cirrhosis of the liver (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Endothelial dysfunction (dpeaa)DE-He213 Hepatic vascular resistance (dpeaa)DE-He213 Nulan, Yelidousi aut Selicean, Sonia aut Wang, Cong aut Gracia-Sancho, Jordi aut Bosch, Jaume (orcid)0000-0003-3414-0055 aut Enthalten in Current hepatitis reports Philadelphia, Pa : Current Science Inc., 2002 22(2023), 1 vom: 11. Feb., Seite 51-66 (DE-627)357168275 (DE-600)2094164-X 1541-0706 nnns volume:22 year:2023 number:1 day:11 month:02 pages:51-66 https://dx.doi.org/10.1007/s11901-023-00598-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 AR 22 2023 1 11 02 51-66
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author	Felli, Eric
spellingShingle	Felli, Eric misc Portal hypertension misc Cirrhosis of the liver misc Fibrosis misc Endothelial dysfunction misc Hepatic vascular resistance Emerging Therapeutic Targets for Portal Hypertension
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topic_title	Emerging Therapeutic Targets for Portal Hypertension Portal hypertension (dpeaa)DE-He213 Cirrhosis of the liver (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Endothelial dysfunction (dpeaa)DE-He213 Hepatic vascular resistance (dpeaa)DE-He213
topic	misc Portal hypertension misc Cirrhosis of the liver misc Fibrosis misc Endothelial dysfunction misc Hepatic vascular resistance
topic_unstemmed	misc Portal hypertension misc Cirrhosis of the liver misc Fibrosis misc Endothelial dysfunction misc Hepatic vascular resistance
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title_sort	emerging therapeutic targets for portal hypertension
title_auth	Emerging Therapeutic Targets for Portal Hypertension
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. © The Author(s) 2023
abstractGer	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. © The Author(s) 2023
abstract_unstemmed	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. © The Author(s) 2023
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title_short	Emerging Therapeutic Targets for Portal Hypertension
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author2	Nulan, Yelidousi Selicean, Sonia Wang, Cong Gracia-Sancho, Jordi Bosch, Jaume
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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. 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Emerging Therapeutic Targets for Portal Hypertension

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