Molecular Basis of Hepatic Encephalopathy: From Experimental to Translational Research

Dear Colleagues,

Hepatic encephalopathy (HE) is defined as a large spectrum of neurological and psychological complications, which are associated with up to 80% of acute and chronic liver diseases (LD) and, in particular cases, with congenital or surgical porta-caval anastomosis, in the absence of hepato-cellular failure. While the etiologies of LD vary from viral hepatitis to liver steatosis, due to alcohol and non-controlled use  of certain drugs like paracetamol, the incidence of LD differs between countries, with over two million deaths annually (representing 4% of total fatalities worldwide). Since the early works of Nicolai Eck (1877), experimental and clinical studies have attempted to define the pathological basis underlying the neuropathology of both acute and chronic HE, leading to the establishment of several theories, including the roles of ammonia, neuroinflammation, manganese neurotoxicity, false neurotransmitters, GABAergic neurotransmission modulation, etc.

I am pleased to invite you to contribute to our Special Issue, entitled, “Molecular Basis of Hepatic Encephalopathy: From Experimental to Translational Research,” which aims to shed light on the recent advances in understanding the neuropathology of HE by providing new, insightful, and solid molecular and cellular mechanisms of HE, based on experimental and clinical evidence, along with an update on the recent progress in HE management and therapies.

Therefore, we are pleased to invite you to submit your manuscripts, which may be original research articles or narrative and systematic reviews. 

I look forward to receiving your contributions.

Dr. Omar EL HIBA
Guest Editor

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