Signaling Pathways in Alcohol Induced Inflammation
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".
Deadline for manuscript submissions: closed (30 July 2021) | Viewed by 3576
Special Issue Editor
Special Issue Information
Dear Colleagues,
Acute and chronic alcohol exposure cause the increased production of reactive oxygen species (ROS) in cells; eventually, it associates with the state of oxidative stress and induces cell damage and death. Excessive alcohol consumption plays a notorious role in instigating inflammation in multiple organs, including vital organs. Chronic alcoholism results in liver inflammation and damage. It is necessary to explore the liver cell types involved in alcohol-mediated liver inflammation, oxidative stress leading to chronic hepatic ailments, as well as its pathogenesis, which involves various intracellular signaling pathways in different cell types. Ample research studies evidently show that the consumption of alcohol induces inflammation in the brain, acute or chronic, long-term alterations in brain functions, and contributes to neurodegeneration. Alcohol-induced neuroinflammation is the prime cause of intercellular and intracellular changes in the brain and, hence, molecular changes in the central nervous system. Alcohol disrupts the blood–brain barrier and affects brain functions. The gut microbiome also plays an important role in various neurological disorders and alcohol-induced inflammation. It is well known that the consumption of alcohol enhances gut-permeability and causes dysfunction, resulting in inflammation in the gastrointestinal tract. In other words, alcohol induces gut dysbiosis and causes endotoxemia, i.e., increased level of lipopolysaccharides (LPS). LPS binds to the TLR4 and triggers downstream signaling, ultimately increasing the inflammatory cytokines and eventually leading to organ damage. Therefore, it is important to understand how gut dysbiosis influences receptor-mediated signaling and affects brain functions. It is equally important to know the salient signaling pathways of alcohol-induced liver inflammation that apparently result in chronic hepatic diseases. This Special Issue aims to reveal the important signaling pathways in alcohol-induced inflammation. I am certain that this section will encompass the outstanding findings from scholarly researchers in this area and will benefit the audience and the related science fraternity. We look forward to your significant contributions to uncover underlying signaling processes.
Dr. Pradeep K. Shukla
Guest Editor
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Keywords
- alcohol
- liver
- inflammation
- neurodegeneration
- gut–brain axis
- signaling pathways
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