New insights into the molecular basis of alcohol abstinence and relapse in alcohol-associated liver disease

Simple item page
dc.catalogadorgrr
dc.contributor.authorDiaz Piga, Luis Antonio
dc.contributor.authorWinder, Gerald Scott
dc.contributor.authorLeggio, Lorenzo
dc.contributor.authorBajaj, Jasmohan S.
dc.contributor.authorBataller, Ramon
dc.contributor.authorArab, Juan Pablo
dc.date.accessioned2023-12-19T14:13:29Z
dc.date.available2023-12-19T14:13:29Z
dc.date.issued2023
dc.description.abstractAlcohol use disorder (AUD) remains a significant public health concern, affecting around 5% of adults worldwide. Novel pathways of damage have been described during the last years, providing insight into the mechanism of injury due to alcohol misuse beyond the direct effect of ethanol byproducts on the liver parenchyma and neurobehavioral mechanisms. Thus, the gut-liver-brain axis and immune system involvement could be therapeutic targets for AUD. In particular, a change in gut microbiota composition and function, especially bile acid homeostasis, and these changes can improve after alcohol cessation. Alcohol can also directly disrupt intestinal and blood-brain barriers. Activation of the immune system can be triggered by intestinal barrier dysfunction and translocation of bacteria, pathogen-associated molecular patterns (such as lipopolysaccharide), cytokines, and damage-associated molecular patterns. These factors in turn promote liver and brain inflammation and progression of liver fibrosis. Other involved mechanisms include oxidative stress, apoptosis, autophagy, and the release of extracellular vesicles and miRNA from hepatocytes. Potential therapeutic targets include gut microbiota (probiotics and fecal microbiota transplantation), neuroinflammatory pathways, as well as neuroendocrine pathways, e.g.: the ghrelin system (ghrelin receptor blockade), incretin mimetics (GLP-1 analogs), and the mineralocorticoid receptor system (spironolactone). In addition, support with psychological and behavioral treatments is essential to address the multiple dimensions of AUD. In the future, a personalized approach considering these novel targets can contribute to significantly decreasing the alcohol-related burden of disease.
dc.fuente.origenWOS
dc.identifier.doi10.1097/HEP.0000000000000645
dc.identifier.eissn1527-3350
dc.identifier.issn0270-9139
dc.identifier.pubmedid37862466
dc.identifier.urihttps://doi.org/10.1097/HEP.0000000000000645
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/75528
dc.identifier.wosidWOS:001110239000001
dc.information.autorucEscuela de Medicina; Diaz Piga, Luis Antonio; S/I; 179253
dc.language.isoen
dc.nota.accesoContenido parcial
dc.publisherLippincott Williams & Wilkins
dc.revistaHepatology
dc.rightsacceso restringido
dc.subjectAlcohol
dc.subjectAlcohol-associated hepatitis
dc.subjectAlcohol use disorders
dc.subjectAlcoholic liver disease
dc.subjectCirrhosis
dc.subjectImmune system
dc.subjectMicrobiota
dc.subjectNeurobiology
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleNew insights into the molecular basis of alcohol abstinence and relapse in alcohol-associated liver disease
dc.typeartículo
sipa.codpersvinculados179253
sipa.trazabilidadWOS;2023-12-16
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
Dïaz_Hepatology_abstract.pdf
Size:
50.73 KB
Format:
Adobe Portable Document Format
Description:
Download
Collections
Artículos de revistas