scholarly journals Chronic liver injury in rats and humans upregulates the novel enzyme angiotensin converting enzyme 2

Gut ◽  
2005 ◽  
Vol 54 (12) ◽  
pp. 1790-1796 ◽  
Author(s):  
G Paizis
Keyword(s):  
Liver Injury ◽  
Angiotensin Converting Enzyme ◽  
Chronic Liver ◽  
The Novel ◽  
Converting Enzyme ◽  
Chronic Liver Injury ◽  
Angiotensin Converting Enzyme 2

Liver fibrosis: a balance of ACEs?

2007 ◽  
Vol 113 (3) ◽  
pp. 109-118 ◽  
Author(s):  
Fiona J. Warner ◽  
John S. Lubel ◽  
Geoffrey W. McCaughan ◽  
Peter W. Angus
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Angiotensin Converting Enzyme ◽  
Transforming Growth Factor ◽  
Tissue Growth ◽  
Chronic Liver ◽  
Converting Enzyme ◽  
Chronic Liver Injury

There is an increasing body of evidence to suggest that the RAS (renin–angiotensin system) contributes to tissue injury and fibrosis in chronic liver disease. A number of studies have shown that components of a local hepatic RAS are up-regulated in fibrotic livers of humans and in experimental animal models. Angiotensin II, the main physiological effector molecule of this system, mediates liver fibrosis by stimulating fibroblast proliferation (myofibroblast and hepatic stellate cells), infiltration of inflammatory cells, and the release of inflammatory cytokines and growth factors such as TGF (transforming growth factor)-β1, IL (interleukin)-1β, MCP (monocyte chemoattractant protein)-1 and connective tissue growth factor. Furthermore, blockade of the RAS by ACE (angiotensin-converting enzyme) inhibitors and angiotensin type 1 receptor antagonists significantly attenuate liver fibrosis in experimental models of chronic liver injury. In 2000 ACE2 (angiotensin-converting enzyme 2), a human homologue of ACE, was identified. ACE2 efficiently degrades angiotensin II to angiotensin-(1–7), a peptide which has recently been shown to have both vasodilatory and tissue protective effects. This suggests that ACE2 and its products may be part of an alternate enzymatic pathway in the RAS, which counterbalances the generation and actions of angiotensin II, the ACE2–angiotensin-(1–7)–Mas axis. This review focuses on the potential roles of the RAS, angiotensin II and ACE2 in chronic liver injury and fibrogenesis.

scholarly journals ACE2 Nascence, trafficking, and SARS-CoV-2 pathogenesis: the saga continues

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Sally Badawi ◽  
Bassam R. Ali
Keyword(s):  
Cell Surface ◽  
Angiotensin Converting Enzyme ◽  
The Novel ◽  
Converting Enzyme ◽  
Post Translational Modifications ◽  
Angiotensin Converting Enzyme 2 ◽  
Viral Attachment ◽  
Novel Coronavirus ◽  
Effective Medication ◽  
Potential Use

AbstractWith the emergence of the novel coronavirus SARS-CoV-2 since December 2019, more than 65 million cases have been reported worldwide. This virus has shown high infectivity and severe symptoms in some cases, leading to over 1.5 million deaths globally. Despite the collaborative and concerted research efforts that have been made, no effective medication for COVID-19 (coronavirus disease-2019) is currently available. SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE2) as an initial mediator for viral attachment and host cell invasion. ACE2 is widely distributed in the human tissues including the cell surface of lung cells which represent the primary site of the infection. Inhibiting or reducing cell surface availability of ACE2 represents a promising therapy for tackling COVID-19. In this context, most ACE2–based therapeutic strategies have aimed to tackle the virus through the use of angiotensin-converting enzyme (ACE) inhibitors or neutralizing the virus by exogenous administration of ACE2, which does not directly aim to reduce its membrane availability. However, through this review, we present a different perspective focusing on the subcellular localization and trafficking of ACE2. Membrane targeting of ACE2, and shedding and cellular trafficking pathways including the internalization are not well elucidated in literature. Therefore, we hereby present an overview of the fate of newly synthesized ACE2, its post translational modifications, and what is known of its trafficking pathways. In addition, we highlight the possibility that some of the identified ACE2 missense variants might affect its trafficking efficiency and localization and hence may explain some of the observed variable severity of SARS-CoV-2 infections. Moreover, an extensive understanding of these processes is necessarily required to evaluate the potential use of ACE2 as a credible therapeutic target.

Temporospatial expression of endothelin converting enzyme-1 in acute and chronic liver injury and fibrogenesis

2000 ◽  
Vol 118 (4) ◽  
pp. A989 ◽  
Author(s):  
Jae-Jin Cho ◽  
Nik Sadlaczek ◽  
Hans D. Orzechowski ◽  
Heiko Funke-Kaiser ◽  
Martin Rühl ◽  
...  
Keyword(s):  
Liver Injury ◽  
Chronic Liver ◽  
Converting Enzyme ◽  
Chronic Liver Injury ◽  
Endothelin Converting Enzyme

322 Chronic liver injury up-regulates the novel enzyme ACE2 in rat and man

2004 ◽  
Vol 40 ◽  
pp. 98
Author(s):  
G. Paizis ◽  
C. Tikellis ◽  
M.E. Cooper ◽  
J.M. Pete ◽  
L.M. Burrell ◽  
...  
Keyword(s):  
Liver Injury ◽  
Chronic Liver ◽  
The Novel ◽  
Chronic Liver Injury

scholarly journals COVID-19 and Liver injury: hepatology perspectives

2020 ◽  
Vol 2 (3) ◽  
pp. 01-04
Author(s):  
Irami Filho
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Liver Damage ◽  
Clinical Manifestations ◽  
Protein S ◽  
Clinical Syndrome ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2

SARS-CoV-2, a severe acute respiratory syndrome caused by Coronavirus 2, discovered in 2019 in China, is responsible for the current pandemic declared by the WHO since March 2020. The clinical syndrome caused by Covid-19 has a broad spectrum of severity. The most common clinical manifestations are fever, dry cough, dyspnea, fatigue, and anosmia. The virus binds to receptors for angiotensin-converting enzyme 2 (ECA2) and serine protease TMPRSS2 for protein S initiation, which are expressed not only in the lungs but also in the liver, colonic, esophageal and biliary epithelial cells. In this context, the liver is a potential target for COVID-19 infection. Liver damage occurs during the course and treatment of viral infection in patients with or without previous liver disease. Therefore, the characteristics of liver injury associated with COVID-19 were reviewed based on research related, in the context of the pandemic.

scholarly journals ACE2 Nascence, Trafficking and SARS-CoV-2 Pathogenesis: The Saga Continues

2020 ◽  
Author(s):  
Sally Badawi ◽  
Bassam Ali
Keyword(s):  
Cell Surface ◽  
Angiotensin Converting Enzyme ◽  
Virus Disease ◽  
The Novel ◽  
Converting Enzyme ◽  
Post Translational Modifications ◽  
Angiotensin Converting Enzyme 2 ◽  
Viral Attachment ◽  
Corona Virus ◽  
Potential Use

With the emergence of the novel corona virus SARS-CoV-2 since December 2019, more than 43 million cases have been reported worldwide. This virus has shown high infectivity and severe symptoms in some cases leading to over 1 million deaths globally. Despite the collaborative and concerted research efforts that has been made, no effective treatment for COVID-19 (corona virus disease-2019) is currently available. SARS-CoV-2 uses the angiotensin converting enzyme 2 (ACE2) as an initial mediator for viral attachment and host cell invasion. ACE2 is widely distributed in human tissues including the cell surface of lung cells which represent the primary site of the infection. Inhibiting or reducing cell surface availability of ACE2 represents a promising therapy for tackling COVID-19. In this context, most ACE2–based therapeutic strategies have aimed to achieve this through the use of angiotensin converting enzyme (ACE) inhibitors or neutralizing the virus by exogenous administration of ACE2. However, through this review, we present another perspective focusing on the subcellular localization and trafficking of ACE2. Membrane targeting of ACE2, shedding and its cellular trafficking pathways including internalization are not well elucidated. Therefore, hereby we present an overview on the fate of newly synthesized ACE2, its post translational modifications, what is known of its trafficking pathways. In addition, we highlight the possibility that some of the identified ACE2 missense variants might affect its trafficking efficiency and localization and hence may explain some of the observed variable severity of SARS-CoV-2 infections. Extensive understanding of these processes is necessary to evaluate the potential use of ACE2 as a credible therapeutic target.

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