ReviewRedox biology2014
Mitochondrial cholesterol accumulation in alcoholic liver disease: Role of ASMase and endoplasmic reticulum stress.
Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 75 citations in OpenAlex.
- Article
- The pivotal role of mitochondria in the pathogenesis and treatment of liver failure: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Alcohol-Induced Oxidative Stress and Gut-Liver-Brain Crosstalk: Expanding the Paradigm from ALD to MetALD.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondria and Alcohol-Associated Liver Disease: Pathogenic Role and Target for Therapy.Seminars in liver disease · 2025Review
- New Insights into the Pathogenesis of Alcoholic Liver Disease Based on Global Research.Digestive diseases and sciences · 2025Review
- Cholesterol Accumulation Caused Oxidative Stress Associated With Impaired Antioxidant Capability and Mitochondrial Function in the Liver of Nile Tilapia.Aquaculture nutrition · 2025Article
- Cardiometabolic risk factors in MASLD patients with HCC: the other side of the coin.Frontiers in endocrinology · 2024Review
- Anti-miR-873-5p improves alcohol-related liver disease by enhancing hepatic deacetylation via SIRT1.JHEP reports : innovation in hepatology · 2024Article
- Phosphoglycerate mutase 5 aggravates alcoholic liver disease through disrupting VDAC-1-dependent mitochondrial integrity.International journal of medical sciences · 2024Article
- Article
- The Crosstalk between Mesenchymal Stromal/Stem Cells and Hepatocytes in Homeostasis and under Stress.International journal of molecular sciences · 2023Review
- A new perspective on mesenchymal stem cell-based therapy for liver diseases: restoring mitochondrial function.Cell communication and signaling : CCS · 2023Review
- Zonal expression of StARD1 and oxidative stress in alcoholic-related liver disease.Journal of lipid research · 2023Article
- Integrated multi-dimensional analysis highlights DHCR7 mutations involving in cholesterol biosynthesis and contributing therapy of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Potential Therapeutic Implication of Herbal Medicine in Mitochondria-Mediated Oxidative Stress-Related Liver Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Cholesterol Induces Oxidative Stress, Mitochondrial Damage and Death in Hepatic Stellate Cells to Mitigate Liver Fibrosis in Mice Model of NASH.Antioxidants (Basel, Switzerland) · 2022Article
- Intracellular Cholesterol Synthesis and Transport.Frontiers in cell and developmental biology · 2022Review
- Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC.Biomedicines · 2021Review
- From Liver Fat to Cancer: Perils of the Western Diet.Cancers · 2021Review
- STARD1 Functions in Mitochondrial Cholesterol Metabolism and Nascent HDL Formation. Gene Expression and Molecular mRNA Imaging Show Novel Splicing and a 1:1 Mitochondrial Association.Frontiers in endocrinology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alcoholic liver disease (ALD) is a major cause of chronic liver disease and a growing health concern in theworld. While the pathogenesis of ALD is poorly characterized key players identified in experimental models and patients, such as perturbations in mitochondrial structure and function, selective loss of antioxidant defense and susceptibility to inflammatory cytokines, contribute to ALD progression. Both oxidative stress and mitochondrial dysfunction compromise essential cellular functions and energy generation and hence are important pathogenic mechanisms of ALD. An important process mediating the mitochondrial disruption induced by alcohol intake is the trafficking of cholesterol to mitochondria, mediated by acid sphingomyelinase-induced endoplasmic reticulum stress, which contributes to increased cholesterol synthesis and StARD1upregulation. Mitochondrial cholesterol accumulation not only sensitizes to oxidative stress but it can contribute to the metabolic reprogramming in ALD, manifested by activation of the hypoxia inducible transcription factor 1 and stimulation of glycolysis and lactate secretion. Thus, a better understanding of the mechanisms underlying alcohol-mediated mitochondrial impairment and oxidative stress may lead to the identification of novel treatments for ALD. The present review briefly summarizes current knowledge on the cellular and molecular mechanisms contributing to alcohol-induced mitochondrial dysfunction and cholesterol accumulation and provides insights for potential therapeutic targets in ALD.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.