by Aleksander J. Nowak, Borna Relja
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.
Reference:
The Impact of Acute or Chronic Alcohol Intake on the NF-κB Signaling Pathway in Alcohol-Related Liver Disease (Aleksander J. Nowak, Borna Relja), In International journal of molecular sciences, volume 21, 2020.
Bibtex Entry:
@article{nowak_impact_2020,
	title = {The {Impact} of {Acute} or {Chronic} {Alcohol} {Intake} on the {NF}-κ{B} {Signaling} {Pathway} in  {Alcohol}-{Related} {Liver} {Disease}},
	volume = {21},
	issn = {1422-0067 1422-0067},
	doi = {10.3390/ijms21249407},
	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.},
	language = {eng},
	number = {24},
	journal = {International journal of molecular sciences},
	author = {Nowak, Aleksander J. and Relja, Borna},
	month = dec,
	year = {2020},
	pmid = {33321885},
	pmcid = {PMC7764163},
	keywords = {A20, acute alcohol intake, Alcohol Drinking/adverse effects/*metabolism, alcoholic liver disease, Animals, chronic alcohol intake, Ethanol/pharmacokinetics/*toxicity, Humans, immunology, Liver Diseases, Alcoholic/*metabolism, Liver/drug effects/*metabolism, NF-kappa B/*metabolism, nuclear factor kappa B, OTUB-1, Signal Transduction, signaling}
}