Pub Date : 2021-07-28DOI: 10.5772/intechopen.96551
L. Iliescu
The development of direct-acting antiviral (DAA) therapies in chronic HCV infection has been associated with increased expectations regarding the prognosis of this infection in the medical community, as the possibility of HCV eradication is now in sight. While the cure of the HVC infection has been associated with a dramatic decrease in its systemic complications, the impact on the progression of the liver disease, especially in patients with cirrhosis, is still controversial. Furthermore, the risk of developing hepatocellular carcinoma (HCC) after direct-acting antiviral therapy is debatable, with studies presenting an increased prevalence of HCC early after the introduction of these therapies, as well as newer contradicting studies. This chapter aims to examine the current literature data available regarding the impact of new HCV therapies in the incidence and prognosis of hepatocellular carcinoma.
{"title":"Hepatocellular Carcinoma and Antiviral Therapies in HCV Chronic Infection","authors":"L. Iliescu","doi":"10.5772/intechopen.96551","DOIUrl":"https://doi.org/10.5772/intechopen.96551","url":null,"abstract":"The development of direct-acting antiviral (DAA) therapies in chronic HCV infection has been associated with increased expectations regarding the prognosis of this infection in the medical community, as the possibility of HCV eradication is now in sight. While the cure of the HVC infection has been associated with a dramatic decrease in its systemic complications, the impact on the progression of the liver disease, especially in patients with cirrhosis, is still controversial. Furthermore, the risk of developing hepatocellular carcinoma (HCC) after direct-acting antiviral therapy is debatable, with studies presenting an increased prevalence of HCC early after the introduction of these therapies, as well as newer contradicting studies. This chapter aims to examine the current literature data available regarding the impact of new HCV therapies in the incidence and prognosis of hepatocellular carcinoma.","PeriodicalId":91047,"journal":{"name":"Advances in hepatology","volume":"280 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75786358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-28DOI: 10.5772/intechopen.97698
Arshpal Gill, Ra’ed Nassar, Ruby Sangha, Mohammed Abureesh, D. Gurala, Zeeshan Zia, Rachelle Hamadi, S. El‐Sayegh
Hepatorenal Syndrome (HRS) is an important condition for clinicians to be aware of in the presence of cirrhosis. In simple terms, HRS is defined as a relative rise in creatinine and relative drop in serum glomerular filtration rate (GFR) alongside renal plasma flow (RPF) in the absence of other competing etiologies of acute kidney injury (AKI) in patients with hepatic cirrhosis. It represents the end stage complication of decompensated cirrhosis in the presence of severe portal hypertension, in the absence of prerenal azotemia, acute tubular necrosis or others. It is a diagnosis of exclusion. The recognition of HRS is of paramount importance for clinicians as it carries a high mortality rate and is an indication for transplantation. Recent advances in understanding the pathophysiology of the disease improved treatment approaches, but the overall prognosis remains poor, with Type I HRS having an average survival under 2 weeks. Generally speaking, AKI and renal failure in cirrhotic patients carry a very high mortality rate, with up to 60% mortality rate for patients with renal failure and cirrhosis and 86.6% of overall mortality rates of patients admitted to the intensive care unit. Of the various etiologies of renal failure in cirrhosis, HRS carries a poor prognosis among cirrhotic patients with acute kidney injury. HRS continues to pose a diagnostic challenge. AKI can be either pre-renal, intrarenal or postrenal. Prerenal causes include hypovolemia, infection, use of vasodilators and functional due to decreased blood flow to the kidney, intra-renal such as glomerulopathy, acute tubular necrosis and post-renal such as obstruction. Patients with cirrhosis are susceptible to developing renal impairment. HRS may be classified as Type 1 or rapidly progressive disease, and Type 2 or slowly progressive disease. There are other types of HRS, but this chapter will focus on Type 1 HRS and Type 2 HRS. HRS is considered a functional etiology of acute kidney injury as there is an apparent lack of nephrological parenchymal damage. It is one several possibilities for acute kidney injury in patients with both acute and chronic liver disease. Acute kidney injury (AKI) is one of the most severe complications that could occur with cirrhosis. Up to 50% of hospitalized patients with cirrhosis can suffer from acute kidney injury, and as mentioned earlier an AKI in the presence of cirrhosis in a hospitalized patient has been associated with nearly a 3.5-fold increase in mortality. The definition of HRS will be discussed in this chapter, but it is characterized specifically as a form of acute kidney injury that occurs in patients with advanced liver cirrhosis which results in a reduction in renal blood flow, unresponsive to fluids this occurs in the setting of portal hypertension and splanchnic vasodilation. This chapter will discuss the incidence of HRS, recognizing HRS, focusing mainly on HRS Type I and Type II, recognizing competing etiologies of renal impairment in
{"title":"Hepatorenal Syndrome","authors":"Arshpal Gill, Ra’ed Nassar, Ruby Sangha, Mohammed Abureesh, D. Gurala, Zeeshan Zia, Rachelle Hamadi, S. El‐Sayegh","doi":"10.5772/intechopen.97698","DOIUrl":"https://doi.org/10.5772/intechopen.97698","url":null,"abstract":"Hepatorenal Syndrome (HRS) is an important condition for clinicians to be aware of in the presence of cirrhosis. In simple terms, HRS is defined as a relative rise in creatinine and relative drop in serum glomerular filtration rate (GFR) alongside renal plasma flow (RPF) in the absence of other competing etiologies of acute kidney injury (AKI) in patients with hepatic cirrhosis. It represents the end stage complication of decompensated cirrhosis in the presence of severe portal hypertension, in the absence of prerenal azotemia, acute tubular necrosis or others. It is a diagnosis of exclusion. The recognition of HRS is of paramount importance for clinicians as it carries a high mortality rate and is an indication for transplantation. Recent advances in understanding the pathophysiology of the disease improved treatment approaches, but the overall prognosis remains poor, with Type I HRS having an average survival under 2 weeks. Generally speaking, AKI and renal failure in cirrhotic patients carry a very high mortality rate, with up to 60% mortality rate for patients with renal failure and cirrhosis and 86.6% of overall mortality rates of patients admitted to the intensive care unit. Of the various etiologies of renal failure in cirrhosis, HRS carries a poor prognosis among cirrhotic patients with acute kidney injury. HRS continues to pose a diagnostic challenge. AKI can be either pre-renal, intrarenal or postrenal. Prerenal causes include hypovolemia, infection, use of vasodilators and functional due to decreased blood flow to the kidney, intra-renal such as glomerulopathy, acute tubular necrosis and post-renal such as obstruction. Patients with cirrhosis are susceptible to developing renal impairment. HRS may be classified as Type 1 or rapidly progressive disease, and Type 2 or slowly progressive disease. There are other types of HRS, but this chapter will focus on Type 1 HRS and Type 2 HRS. HRS is considered a functional etiology of acute kidney injury as there is an apparent lack of nephrological parenchymal damage. It is one several possibilities for acute kidney injury in patients with both acute and chronic liver disease. Acute kidney injury (AKI) is one of the most severe complications that could occur with cirrhosis. Up to 50% of hospitalized patients with cirrhosis can suffer from acute kidney injury, and as mentioned earlier an AKI in the presence of cirrhosis in a hospitalized patient has been associated with nearly a 3.5-fold increase in mortality. The definition of HRS will be discussed in this chapter, but it is characterized specifically as a form of acute kidney injury that occurs in patients with advanced liver cirrhosis which results in a reduction in renal blood flow, unresponsive to fluids this occurs in the setting of portal hypertension and splanchnic vasodilation. This chapter will discuss the incidence of HRS, recognizing HRS, focusing mainly on HRS Type I and Type II, recognizing competing etiologies of renal impairment in ","PeriodicalId":91047,"journal":{"name":"Advances in hepatology","volume":"2015 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86945272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-06-09DOI: 10.5772/intechopen.96975
A. Geerts, S. Lefere
Non-alcoholic fatty liver disease (NAFLD) is a crucial health problem with a prevalence that is increasing concurrently with the obesity epidemic on a global scale. Steatosis, nonalcoholic steatohepatitis (NASH), hepatocellular carcinoma (HCC), cirrhosis, and advanced fibrosis constitute the disease spectrum covered by NAFLD. NASH-related cirrhosis and HCC is currently the second most common indication for liver transplantation. Although lifestyle modifications, especially weight loss, effectively reduces the liver injury in NASH, adherence in the clinical setting is low. Potential treatments for NASH are still under investigation in phase 2–3 studies. Bariatric surgery can improve metabolic components and cause great weight loss. Therefore, bariatric surgery may reverse the pathological liver changes in NAFLD and NASH patients. However, complications such as liver failure after bariatric surgery can occur. This chapter will give an overview of the benefits and pitfalls of bariatric surgery in patients with NAFLD, liver transplant candidates and post-liver transplant patients.
{"title":"The Role of Bariatric Surgery in Fatty Liver","authors":"A. Geerts, S. Lefere","doi":"10.5772/intechopen.96975","DOIUrl":"https://doi.org/10.5772/intechopen.96975","url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is a crucial health problem with a prevalence that is increasing concurrently with the obesity epidemic on a global scale. Steatosis, nonalcoholic steatohepatitis (NASH), hepatocellular carcinoma (HCC), cirrhosis, and advanced fibrosis constitute the disease spectrum covered by NAFLD. NASH-related cirrhosis and HCC is currently the second most common indication for liver transplantation. Although lifestyle modifications, especially weight loss, effectively reduces the liver injury in NASH, adherence in the clinical setting is low. Potential treatments for NASH are still under investigation in phase 2–3 studies. Bariatric surgery can improve metabolic components and cause great weight loss. Therefore, bariatric surgery may reverse the pathological liver changes in NAFLD and NASH patients. However, complications such as liver failure after bariatric surgery can occur. This chapter will give an overview of the benefits and pitfalls of bariatric surgery in patients with NAFLD, liver transplant candidates and post-liver transplant patients.","PeriodicalId":91047,"journal":{"name":"Advances in hepatology","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88423406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-04-05DOI: 10.5772/INTECHOPEN.96910
R. Vaca, B. Vairappan, Tomás Cortés Espinoza, J. A. S. Cuenca, C. Cassani, Brenda Maldonado Arriaga, C. Gerrard, Diana Selene Morgan Penagos, P. Terán, V. C. Sánchez
Changes in intestinal permeability have been determined to influence secondary inflammatory reactions and clinical manifestations such as spontaneous bacterial peritonitis (SBP) secondary to cirrhosis. As of yet, no in-depth exploration of the changes in the microbiota and how this influences cirrhosis to differ from clinically more severe cases than others has not begun. However, at the level of pathophysiological mechanism, it must be taken into account that due to the abuse of substances such as alcohol and chronic fatty liver disease, changes in the bacterial composition and intestinal permeability are induced. This set of changes in the bacterial composition (microbiome) and modification of the intestinal permeability could be related to the presence of ascites and spontaneous peritonitis secondary to cirrhosis, being of relevance the knowledge of the mechanisms underlying this phenomenon, as well as clinical manifestation. Prophylaxis and antibiotic treatment of SBP requires clinical knowledge for the treatment decisions based mainly on the presence of ascitic fluid, accompanied of risk factors, laboratory indexes such as PMN count and culture results, in order to determine the kind of molecule that will help to the SBP recovery or to amelioration symptoms, always taking care of not exceed the antibiotic consumption and restoring the microbiome imbalance.
{"title":"Spontaneous Bacterial Peritonitis: Physiopathological Mechanism and Clinical Manifestations","authors":"R. Vaca, B. Vairappan, Tomás Cortés Espinoza, J. A. S. Cuenca, C. Cassani, Brenda Maldonado Arriaga, C. Gerrard, Diana Selene Morgan Penagos, P. Terán, V. C. Sánchez","doi":"10.5772/INTECHOPEN.96910","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.96910","url":null,"abstract":"Changes in intestinal permeability have been determined to influence secondary inflammatory reactions and clinical manifestations such as spontaneous bacterial peritonitis (SBP) secondary to cirrhosis. As of yet, no in-depth exploration of the changes in the microbiota and how this influences cirrhosis to differ from clinically more severe cases than others has not begun. However, at the level of pathophysiological mechanism, it must be taken into account that due to the abuse of substances such as alcohol and chronic fatty liver disease, changes in the bacterial composition and intestinal permeability are induced. This set of changes in the bacterial composition (microbiome) and modification of the intestinal permeability could be related to the presence of ascites and spontaneous peritonitis secondary to cirrhosis, being of relevance the knowledge of the mechanisms underlying this phenomenon, as well as clinical manifestation. Prophylaxis and antibiotic treatment of SBP requires clinical knowledge for the treatment decisions based mainly on the presence of ascitic fluid, accompanied of risk factors, laboratory indexes such as PMN count and culture results, in order to determine the kind of molecule that will help to the SBP recovery or to amelioration symptoms, always taking care of not exceed the antibiotic consumption and restoring the microbiome imbalance.","PeriodicalId":91047,"journal":{"name":"Advances in hepatology","volume":"09 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86360254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-12DOI: 10.5772/INTECHOPEN.96155
A. Delik, Y. Ülger
Chronic liver disease and decompensated cirrhosis are the major causes of morbidity and mortality in the world. According to current data, deaths due to liver cirrhosis constitute 2.4% of the total deaths worldwide. Cirrhosis is characterized by hepatocellular damage that leads to fibrosis and regenerative nodules in the liver. The most common causes of cirrhosis include alcohol consumption, hepatitis C, hepatitis B, and non-alcoholic fatty liver disease. Dysbiosis and intestinal bacterial overgrowth play a role in the development of complications of cirrhosis through translocation. In liver cirrhosis, ascites, gastrointestinal variceal bleeding, spontaneous bacterial peritonitis infection, hepatic encephalopathy, hepatorenal syndrome, hepatocelluler carcinoma are the most common complications. In addition, there are refractory ascites, hyponatremia, acute on-chronic liver failure, relative adrenal insufficiency, cirrhotic cardiomyopathy, hepatopulmonary syndrome and portopulmonary hypertension. In the primary prophylaxis of variceal bleeding, non-selective beta blockers or endoscopic variceal ligation are recommended for medium and large variceal veins. In current medical treatment, vasoactive agents, antibiotics, blood transfusion, endoscopic band ligation are the standard approach in the treatment of acute variceal bleeding. Sodium-restricted diet, diuretics and large-volume paracentesis are recommended in the management of ascites. In the treatment of hepatic encephalopathy, lactulose, branched chain amino acids, rifaximin and L-ornithine L-aspartate can be used. New therapeutic approaches such as ornithine phenyl acetate spherical carbon and fecal microbiota transplantation have shown beneficial effects on hepatic encephalopathy symptoms. In addition to their antioxidative, anti-proliferative and anti-inflammatory properties, statins have been shown to reduce the risk of decompensation and death by reducing portal pressure in compensated cirrhosis. In the treatment of liver failure, some artificial liver devices such as molecular adsorbent recirculating system, the single albumin dialysis system, fractionated plasma separation and adsorption are used until transplantation or regeneration. The purpose of this chapter is to review the most up-to-date information on liver cirrhosis and to explain the complications assessment, current management and potential treatment strategies in decompensated cirrhosis.
{"title":"Treatment Approach in Patients with Decompensated Liver Cirrhosis","authors":"A. Delik, Y. Ülger","doi":"10.5772/INTECHOPEN.96155","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.96155","url":null,"abstract":"Chronic liver disease and decompensated cirrhosis are the major causes of morbidity and mortality in the world. According to current data, deaths due to liver cirrhosis constitute 2.4% of the total deaths worldwide. Cirrhosis is characterized by hepatocellular damage that leads to fibrosis and regenerative nodules in the liver. The most common causes of cirrhosis include alcohol consumption, hepatitis C, hepatitis B, and non-alcoholic fatty liver disease. Dysbiosis and intestinal bacterial overgrowth play a role in the development of complications of cirrhosis through translocation. In liver cirrhosis, ascites, gastrointestinal variceal bleeding, spontaneous bacterial peritonitis infection, hepatic encephalopathy, hepatorenal syndrome, hepatocelluler carcinoma are the most common complications. In addition, there are refractory ascites, hyponatremia, acute on-chronic liver failure, relative adrenal insufficiency, cirrhotic cardiomyopathy, hepatopulmonary syndrome and portopulmonary hypertension. In the primary prophylaxis of variceal bleeding, non-selective beta blockers or endoscopic variceal ligation are recommended for medium and large variceal veins. In current medical treatment, vasoactive agents, antibiotics, blood transfusion, endoscopic band ligation are the standard approach in the treatment of acute variceal bleeding. Sodium-restricted diet, diuretics and large-volume paracentesis are recommended in the management of ascites. In the treatment of hepatic encephalopathy, lactulose, branched chain amino acids, rifaximin and L-ornithine L-aspartate can be used. New therapeutic approaches such as ornithine phenyl acetate spherical carbon and fecal microbiota transplantation have shown beneficial effects on hepatic encephalopathy symptoms. In addition to their antioxidative, anti-proliferative and anti-inflammatory properties, statins have been shown to reduce the risk of decompensation and death by reducing portal pressure in compensated cirrhosis. In the treatment of liver failure, some artificial liver devices such as molecular adsorbent recirculating system, the single albumin dialysis system, fractionated plasma separation and adsorption are used until transplantation or regeneration. The purpose of this chapter is to review the most up-to-date information on liver cirrhosis and to explain the complications assessment, current management and potential treatment strategies in decompensated cirrhosis.","PeriodicalId":91047,"journal":{"name":"Advances in hepatology","volume":"2677 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88768572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-04DOI: 10.5772/INTECHOPEN.95995
A. Frosi
Chronic infection with the hepatitis C virus (HCV) is a major cause of liver disease worldwide and is also responsible for extrahepatic manifestations (EHM) involving many different organs and apparatus: skin, salivary glands, eyes, thyroid, kidneys, peripheral and central nervous system, and immune system. Mixed cryoglobulinemia is the most frequent, best known and strictly HCV-associated EHM. A significant association between HCV and B-cell Non-Hodgkin-Lymphoma is reported although the incidence of lymphoma among HCV-infected patients overall remains low. HCV-infected patients have increased rates of insulin resistance, diabetes, and atherosclerosis, which may lead to increased cardiovascular disorders. The mechanisms causing the extrahepatic effects of HCV infection are likely multifactorial and may include endocrine effects, HCV replication in extrahepatic cells, or a heightened immune reaction with systemic effects. Because of this associations, it is suggested testing for HCV infection the patients with a clinical condition described as linked to hepatitis C. Conversely, patients diagnosed with HCV infection should have evaluation for a possible EHM. EHM of HCV can be considered an established indication for antiviral treatment with direct acting antivirals, even in the absence of overt liver disease. Successful eradication of HCV can improve and in some cases cure EHM of HCV. B cell depleting agents may be considered to be the best biological target option for patients with more severe EHM in combination with the antivirals.
{"title":"Extrahepatic Manifestations of Hepatitis C Infection","authors":"A. Frosi","doi":"10.5772/INTECHOPEN.95995","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.95995","url":null,"abstract":"Chronic infection with the hepatitis C virus (HCV) is a major cause of liver disease worldwide and is also responsible for extrahepatic manifestations (EHM) involving many different organs and apparatus: skin, salivary glands, eyes, thyroid, kidneys, peripheral and central nervous system, and immune system. Mixed cryoglobulinemia is the most frequent, best known and strictly HCV-associated EHM. A significant association between HCV and B-cell Non-Hodgkin-Lymphoma is reported although the incidence of lymphoma among HCV-infected patients overall remains low. HCV-infected patients have increased rates of insulin resistance, diabetes, and atherosclerosis, which may lead to increased cardiovascular disorders. The mechanisms causing the extrahepatic effects of HCV infection are likely multifactorial and may include endocrine effects, HCV replication in extrahepatic cells, or a heightened immune reaction with systemic effects. Because of this associations, it is suggested testing for HCV infection the patients with a clinical condition described as linked to hepatitis C. Conversely, patients diagnosed with HCV infection should have evaluation for a possible EHM. EHM of HCV can be considered an established indication for antiviral treatment with direct acting antivirals, even in the absence of overt liver disease. Successful eradication of HCV can improve and in some cases cure EHM of HCV. B cell depleting agents may be considered to be the best biological target option for patients with more severe EHM in combination with the antivirals.","PeriodicalId":91047,"journal":{"name":"Advances in hepatology","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77776597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oxidative stress is a common feature observed in a wide spectrum of chronic liver diseases including viral hepatitis, alcoholic, and nonalcoholic steatohepatitis. The nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are emerging as major sources of reactive oxygen species (ROS). Several major isoforms are expressed in the liver, including NOX1, NOX2, and NOX4. While the phagocytic NOX2 has been known to play an important role in Kupffer cell and neutrophil phagocytic activity and inflammation, the nonphagocytic NOX homologues are increasingly recognized as key enzymes in oxidative injury and wound healing. In this review, we will summarize the current advances in knowledge on the regulatory pathways of NOX activation, their cellular distribution, and their role in the modulation of redox signaling in liver diseases.
{"title":"NADPH Oxidases in Chronic Liver Diseases.","authors":"Joy X Jiang, Natalie J Török","doi":"10.1155/2014/742931","DOIUrl":"https://doi.org/10.1155/2014/742931","url":null,"abstract":"<p><p>Oxidative stress is a common feature observed in a wide spectrum of chronic liver diseases including viral hepatitis, alcoholic, and nonalcoholic steatohepatitis. The nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are emerging as major sources of reactive oxygen species (ROS). Several major isoforms are expressed in the liver, including NOX1, NOX2, and NOX4. While the phagocytic NOX2 has been known to play an important role in Kupffer cell and neutrophil phagocytic activity and inflammation, the nonphagocytic NOX homologues are increasingly recognized as key enzymes in oxidative injury and wound healing. In this review, we will summarize the current advances in knowledge on the regulatory pathways of NOX activation, their cellular distribution, and their role in the modulation of redox signaling in liver diseases.</p>","PeriodicalId":91047,"journal":{"name":"Advances in hepatology","volume":"2014 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/742931","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34128972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：