Inflammatory responses on the road from MASH to HCC: pathogenic mechanisms and possible therapeutic strategies – Volume II

This Research Topic is the second volume of the Inflammatory responses on the road from NASH to HCC: pathogenic mechanisms and possible therapeutic strategies, with Volume I getting over 51,000 views Inflammatory responses on the road from NASH to HCC: pathogenic mechanisms and possible therapeutic strategiesMetabolic dysfunction–associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), has emerged as a leading cause of chronic liver disease worldwide, affecting approximately 25–30% of the general population. MASLD represents a spectrum of diseases, ranging from simple steatosis to its progressive form, metabolic dysfunction–associated steatohepatitis (MASH). MASH is often clinically silent but is characterized by hepatocellular injury, lobular and portal inflammation, and variable degrees of fibrosis, which may ultimately progress to cirrhosis and hepatocellular carcinoma (HCC). Despite its growing clinical significance, there are currently no approved pharmacological treatments for advanced-stage MASH or MASH-related HCC.The success of antiviral therapies for viral hepatitis has shifted the global burden of chronic liver disease toward MASLD, underscoring the urgent need for targeted interventions. The cellular and molecular mechanisms driving progression from MASH to HCC remain incompletely understood, representing a major obstacle to effective therapy development. Increasing evidence suggests that chronic hepatic inflammation is a central driver of tumorigenesis. Persistent inflammatory signaling induces oxidative stress and DNA damage, promotes immune cell reprogramming toward immunosuppressive phenotypes, and leads to T-cell exhaustion, collectively creating a microenvironment conducive to malignant transformation and tumor progression.In addition to the MASH–HCC axis, this Research Topic also aims to include inflammatory and immune-mediated mechanisms that drive the development and progression of biliary tract cancers, particularly cholangiocarcinoma (CCA), in the context of chronic liver disease, metabolic dysfunction, and biliary injury. While the etiologies of HCC and CCA differ, both malignancies share common inflammation-driven pathways and immunosuppressive microenvironments that represent promising therapeutic targets.This call for papers aims to bring together innovative research elucidating the role of chronic inflammation in the progression from chronic liver disease to liver cancer, with a primary focus on NASH-driven HCC and an extended scope covering biliary cancers. We welcome studies that provide new insights into:• Cellular and molecular mechanisms perpetuating hepatic inflammation,• Immune cell reprogramming and T-cell dysfunction that promote cancer immune evasion,• Inflammation-driven stromal and immune niches shaping hepatocellular versus biliary tumor development,• Shared and distinct inflammatory pathways between HCC and CCA,• Identification of novel pharmacological targets to counteract chronic inflammation and prevent progression to liver cancer. Topic editors: Veronika Lukacs-Kornek, Salvatore Sutti Source: https://www.frontiersin.org/research-topics/78164/inflammatory-responses-on-the-road-from-mash-to-hcc-pathogenic-mechanisms-and-possible-therapeutic-strategies---volume-ii