Liver disease is highly prevalent in the world. The continuous exposure of the liver to some factors, such as viruses, alcohol, fat, and biotransformed metabolites, among others, can cause hepatic injury, which can lead to inflammation and liver degeneration. When the injury is sustained for a long time, it can cause chronic liver diseases (CLDs), which include a spectrum of disease states ranging from simple steatosis and steatohepatitis (steatosis with inflammation and hepatocyte injury and death) to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Although the clinical manifestations of liver disease are well-described, the mechanisms underlying development of this disease and its progression from steatosis alone to hepatocellular injury to chronic liver disease remain poorly understood. Multiple evidences indicate that oxidative stress and inflammation are the most important pathogenetic events in liver diseases, regardless of the different etiology and natural course. Most if not all the pathogenic insults in the liver can cause oxidative stress, inducing reactive oxygen species (ROS) generation, protein oxidation, and DNA damage. Further, CLDs lead to macrophage overactivation from inflammatory stimuli and increased release of proinflammatory and profibrogenic mediators that contribute to the hepatocyte necrosis and apoptosis. In addition, Kupffer cells (KC) induce activation of the immune system, innate and adaptive, with polymorphonuclear (PMN) leukocytes infiltration, inducible nitric oxide synthase (iNOS) upregulation, and recruitment of lymphocytes through the portal tract, hepatic vein, and sinusoids. In chronic liver diseases, hepatocyte injury triggers hepatic stellate cell (HSC), the major cell type responsible for the progression of liver fibrosis. Following liver injury, multiple physiological processes are altered in HSC including loss of their vitamin A stores, increased cytoskeleton contractility, and the expression of fibrogenic genes. These alterations in HSC are collectively known as HSC “transdifferentiation.” Together, these changes are the cause for the formation of scar tissue observed in fibrotic and cirrhotic livers.

Current therapies in chronic liver diseases are limited and liver transplantation is the only available treatment for end-stage liver disease. Therefore, there is a vital need for novel approaches and therapeutically aligned basic, clinical, and translational research as hepatic damage-related morbidity and mortality continue to exert a substantial toll on the world. Our aim is to bring together novel research and insight views on the role of oxidative stress and inflammation during hepatic diseases. We invite authors to contribute original research articles and review articles that will illustrate and stimulate the fundamental mechanisms as well as clinical treatments for CLDs. Only through a better understanding of the basic pathophysiology underlying the development of steatosis, steatohepatitis, fibrosis, cirrhosis, and HCC can better treatments evolve for liver diseases.

Potential topics include but are not limited to the following:

• Classical mechanisms of liver damage
• Inflammatory response during CLDs
• Sources and triggers of ROS and inflammation during CLDs
• Methods to evaluate oxidative stress and/or inflammation in the liver
• Participation of ROS and/or inflammation on liver diseases spectrum (steatosis, fibrosis, cirrhosis, and/or cancer)
• Participation of oxidative stress in alcoholic and nonalcoholic liver disease
• Recent advances in the treatment of CLDs
• Pharmacological treatments for CLDs
• Traditional and herbal therapy for CLDs
• Diagnosis and management of liver diseases
• Recent advances in transplant surgery
• Other areas of redox biology which may pave the way for further investigations of the ROS/RNS interplay in viral, bacterial, and parasitic disease