Abstract

Ethanol misuse is frequently associated with a multitude of profound medical conditions, contributing to health-, individual- and social-related damage. A particularly dangerous threat from this classification is coined as alcoholic liver disease (ALD), a liver condition caused by prolonged alcohol overconsumption, involving several pathological stages induced by alcohol metabolic byproducts and sustained cellular intoxication. Molecular, pathological mechanisms of ALD principally root in the innate immunity system and are especially associated with enhanced functionality of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. NF-κB is an interesting and convoluted DNA transcription regulator, promoting both anti-inflammatory and pro-inflammatory gene expression. Thus, the abundancy of studies in recent years underlines the importance of NF-κB in inflammatory responses and the mechanistic stimulation of inner molecular motifs within the factor components. Hereby, in the following review, we would like to put emphasis on the correlation between the NF-κB inflammation signaling pathway and ALD progression. We will provide the reader with the current knowledge regarding the chronic and acute alcohol consumption patterns, the molecular mechanisms of ALD development, the involvement of the NF-κB pathway and its enzymatic regulators. Therefore, we review various experimental in vitro and in vivo studies regarding the research on ALD, including the recent active compound treatments and the genetic modification approach. Furthermore, our investigation covers a few human studies.

Highlights

  • Ethanol in the form of various and diversified beverages is one of the world’s most commonly consumed active ingredients in drinks, alongside caffeine [1]

  • A dangerous threat from this classification is coined as alcoholic liver disease (ALD), a liver condition caused by prolonged alcohol overconsumption, involving several pathological stages induced by alcohol metabolic byproducts and sustained cellular intoxication

  • EtOH is mainly oxidized by the cytosol-based enzyme alcohol dehydrogenase (ADH), which converts the hydroxyl-based EtOH compound into its metabolic intermediate ethanal (MeCHO, acetaldehyde), which is characterized by the presence of the functional formyl group [46]

Read more

Summary

Introduction

Ethanol (ethylic alcohol, EtOH) in the form of various and diversified beverages is one of the world’s most commonly consumed active ingredients in drinks, alongside caffeine [1]. The multi-layered pathogenesis of ALD is still not comprehensively understood, especially the direct alterations of signaling pathways in the liver cells, which stimulate an immune response and abundant release of pro-inflammatory factors, including tumor necrosis alpha (TNFα) and interleukin 1-beta (IL-1β) [8]. This leads to the change in expression levels of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), a crucial transcription factor complex [9]. We surveyed the most recent literature papers regarding the topic, contributing to the establishment of a novel discussion environment for possible treatments and research directions in the future of alcoholic liver disease investigations [13]

Review Criteria
Alcohol Intake and Its Influence on the Liver
Alcohol-Related Liver Conditions
Toxicity of Alcohol to the Liver
The Role of NF-κB in the Innate Immune Response
NF-κB Activity Research in Alcohol-Related Liver Injury Animal Models
The Potential Treatment Approach for Alcohol-Induced Liver Inflammation
Genetic Manipulations
Further Studies
Findings
Discussion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call