Oxidative Stress in Liver Disease and Cardiovascular Risk

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 1264

Special Issue Editors


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Guest Editor
Internal Medicine Department, Universidad de La Laguna, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain
Interests: liver disease; alcoholic hepatitis; liver injury; alcohol; alcohol and disease
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Unit of Physiology, Department of Basic Medical Sciences, University of La Laguna, 38200 Santa Cruz de Tenerife, Spain
Interests: alcohol and disease; oxidative stress; cardiovascular diseases; alcoholic liver disease

Special Issue Information

Dear Colleagues,

Non-alcoholic fatty liver disease (NAFLD) is a pathological spectrum ranging from simple steatosis to steatohepatitis, in the absence of harmful alcohol consumption, and is considered the hepatic manifestation of the metabolic syndrome. Recent studies indicate that it is closely related to cardiovascular disease, especially thickening of the carotid artery intima-media layer, as a morphostructural manifestation of the presence of subclinical atheromatosis. In relation to pathogenesis, oxidative stress has been identified as the common link between both entities.

Moreover, oxidative stress plays an important role in the development of alcohol-induced liver damage. Thus, alcohol metabolism via alcohol dehydrogenase leads to the formation of acetaldehyde and ROS, increased lipid peroxidation and decreased antioxidant mechanisms.

NAFLD and alcoholic liver disease are associated with increased cardiovascular risk. NAFLD causes a systemic proinflammatory state and increased oxidative stress, leading to endothelial dysfunction and thus increased cardiovascular risk in asymptomatic individuals. Alcohol itself is toxic to the cardiovascular system. Patients who consume large amounts of alcohol can development cardiac arrhythmias, alcoholic dilated cardiomyopathy or hypertension, among others. In alcoholic liver disease, in addition to REDOX imbalance, there is increased gastrointestinal permeability, with the passage of lipopolysaccharide from Gram-negative bacteria into the portal circulation. This lipopolysaccharide stimulates the hepatic Kuppfer cell, triggering intense cytokine release and leading to an underlying proinflammatory situation.

This Special Issue aims to provide a platform for molecular mechanistic research on oxidative stress in liver disease, with a special focus on potential treatments and novel pathogenic pathways involved in cardiovascular risk in patients with liver disease. We warmly welcome your submissions of original papers and reviews based on results from molecular viewpoints.

Dr. María Candelaria Martín-González
Dr. Pedro Abreu-González
Guest Editors

Manuscript Submission Information

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Keywords

  • non-alcoholic fatty liver disease
  • NAFLD
  • alcohol liver disease
  • cardiovascular risk
  • oxidative stress
  • ROS
  • subclinical atheromatosis
  • REDOX imbalance
  • antioxidants
  • lipid peroxidation
  • cardiovascular disease
  • metabolic syndrome

Published Papers (1 paper)

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Research

17 pages, 35972 KiB  
Article
17β-Estradiol (E2) Upregulates the ERα/SIRT1/PGC-1α Signaling Pathway and Protects Mitochondrial Function to Prevent Bilateral Oophorectomy (OVX)-Induced Nonalcoholic Fatty Liver Disease (NAFLD)
by Ying Tian, Xinyu Hong, Yuan Xie, Zaixin Guo and Qi Yu
Antioxidants 2023, 12(12), 2100; https://doi.org/10.3390/antiox12122100 - 12 Dec 2023
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Abstract
Premature menopause is associated with an increased prevalence of nonalcoholic fatty liver disease (NAFLD). Menopausal hormone therapy (MHT) has been widely used in clinical practice and has the potential to protect mitochondrial function and alleviate NAFLD. After bilateral oophorectomy (OVX), female rats without [...] Read more.
Premature menopause is associated with an increased prevalence of nonalcoholic fatty liver disease (NAFLD). Menopausal hormone therapy (MHT) has been widely used in clinical practice and has the potential to protect mitochondrial function and alleviate NAFLD. After bilateral oophorectomy (OVX), female rats without 17β-estradiol (E2) intervention developed NAFLD, whereas E2 supplementation was effective in preventing NAFLD in female rats. The altered pathways and cellular events from both comparison pairs, namely, the OVX vs. sham group and the OVX vs. E2 group, were assessed using transcriptomic analysis. KEGG pathways enriched by both transcriptomic and metabolomic analyses strongly suggest that oxidative phosphorylation is a vital pathway that changes during the development of NAFLD and remains unchanged when E2 is applied. Liver tissue from the OVX-induced NAFLD group exhibited increased lipid peroxidation, impaired mitochondria, and downregulated ERα/SIRT1/PGC-1α expression. An in vitro study indicated that the protective effect of E2 treatment on hepatic steatosis could be abolished when ERα or SIRT1 was selectively inhibited. This damage was accompanied by reduced mitochondrial complex activity and increased lipid peroxidation. The current research indicates that E2 upregulates the ERα/SIRT1/PGC-1α signaling pathway and protects mitochondrial function to prevent OVX-induced NAFLD. Full article
(This article belongs to the Special Issue Oxidative Stress in Liver Disease and Cardiovascular Risk)
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