Non-alcoholic fatty liver disease (NAFLD) is a growing cause of chronic liver disease worldwide, with a global prevalence accounting for 25-30% of the general population. NAFLD is a generic term referring to a wide spectrum of diseases ranging from simple steatosis to its advanced stage, non-alcoholic steatohepatitis (NASH). NASH is often an asymptomatic pathological condition characterized by hepatocellular necrosis and lobular and portal inflammation with or without fibrosis. NASH can further progress to cirrhosis and, in some cases, to hepatocellular carcinoma (HCC). Despite the clinical relevance of NAFLD, there are no approved pharmacological treatments for NASH and NASH-related HCC so far.
The introduction of effective therapies for viral hepatitis shifted the paradigm of chronic liver diseases, leaving NAFLD the record of most frequent hepatic lesion worldwide. And the lack of specific treatments contributes to making this picture even worse. In addition, the cellular and molecular mechanisms underlying the transition from NASH to HCC are still poorly characterized. Therefore, it makes it arduous fine-tuning effective pharmacological treatments to restrain disease progression toward carcinogenesis. However, the observation that HCC arises in the context of chronically inflamed livers suggested that inflammatory reactions may act as the driving force, favouring the transition from NASH to HCC. The current view sees chronic inflammation as a fundamental player promoting cancer initiation through the induction of oxidative stress and DNA damage, thus sustaining cellular transformation. Within chronically inflamed livers, immune cells undergo functional reprogramming, acquiring immunosuppressive properties that, together with regulatory-T cell expansion and T-cell exhaustion following persistent antigen stimulation, establish a cancer-prone microenvironment where transformed cells can grow undisturbed.
The present call for papers aims to gather innovative research focusing on the contribution of chronic inflammatory responses in the transition from NASH to NASH-related HCC. The articles should provide novel insights regarding cellular and molecular mechanisms responsible for the perpetuation of hepatic inflammatory responses, immune cell reprogramming toward immunosuppressive phenotypes and T-cell exhaustion, engendering cancer immune evasion. Special attention will also be dedicated to reports concerning the identification of novel pharmacological targets that can be exploited to counteract NASH-associated inflammation,
Non-alcoholic fatty liver disease (NAFLD) is a growing cause of chronic liver disease worldwide, with a global prevalence accounting for 25-30% of the general population. NAFLD is a generic term referring to a wide spectrum of diseases ranging from simple steatosis to its advanced stage, non-alcoholic steatohepatitis (NASH). NASH is often an asymptomatic pathological condition characterized by hepatocellular necrosis and lobular and portal inflammation with or without fibrosis. NASH can further progress to cirrhosis and, in some cases, to hepatocellular carcinoma (HCC). Despite the clinical relevance of NAFLD, there are no approved pharmacological treatments for NASH and NASH-related HCC so far.
The introduction of effective therapies for viral hepatitis shifted the paradigm of chronic liver diseases, leaving NAFLD the record of most frequent hepatic lesion worldwide. And the lack of specific treatments contributes to making this picture even worse. In addition, the cellular and molecular mechanisms underlying the transition from NASH to HCC are still poorly characterized. Therefore, it makes it arduous fine-tuning effective pharmacological treatments to restrain disease progression toward carcinogenesis. However, the observation that HCC arises in the context of chronically inflamed livers suggested that inflammatory reactions may act as the driving force, favouring the transition from NASH to HCC. The current view sees chronic inflammation as a fundamental player promoting cancer initiation through the induction of oxidative stress and DNA damage, thus sustaining cellular transformation. Within chronically inflamed livers, immune cells undergo functional reprogramming, acquiring immunosuppressive properties that, together with regulatory-T cell expansion and T-cell exhaustion following persistent antigen stimulation, establish a cancer-prone microenvironment where transformed cells can grow undisturbed.
The present call for papers aims to gather innovative research focusing on the contribution of chronic inflammatory responses in the transition from NASH to NASH-related HCC. The articles should provide novel insights regarding cellular and molecular mechanisms responsible for the perpetuation of hepatic inflammatory responses, immune cell reprogramming toward immunosuppressive phenotypes and T-cell exhaustion, engendering cancer immune evasion. Special attention will also be dedicated to reports concerning the identification of novel pharmacological targets that can be exploited to counteract NASH-associated inflammation,
