ReviewCurrent molecular pharmacology2017
The Activation and Function of Autophagy in Alcoholic Liver Disease.
Review in Current molecular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 25 citations in OpenAlex.
- Mechanism and regulation of mitophagy in liver diseases: a review.Frontiers in cell and developmental biology · 2025Review
- Autophagy in Disease Onset and Progression.Aging and disease · 2024Review
- Alcohol-related liver disease (ALD): current perspectives on pathogenesis, therapeutic strategies, and animal models.Frontiers in pharmacology · 2024Review
- Distinct Types of Cell Death and Implications in Liver Diseases: An Overview of Mechanisms and Application.Journal of clinical and translational hepatology · 2023Review
- Hepatic Macrophages as Targets for the MSC-Based Cell Therapy in Non-Alcoholic Steatohepatitis.Biomedicines · 2023Review
- Autophagy, Oxidative Stress, and Alcoholic Liver Disease: A Systematic Review and Potential Clinical Applications.Antioxidants (Basel, Switzerland) · 2023Review
- Emerging mechanistic insights of selective autophagy in hepatic diseases.Frontiers in pharmacology · 2023Review
- Therapeutic regulation of autophagy in hepatic metabolism.Acta pharmaceutica Sinica. B · 2022Review
- Cell Death in Liver Diseases: A Review.International journal of molecular sciences · 2020Review
- Daily Ethanol Drinking Followed by an Abstinence Period Impairs Bone Marrow Niche and Mitochondrial Function of Hematopoietic Stem/Progenitor Cells in Rhesus Macaques.Alcoholism, clinical and experimental research · 2020Article
- Dysregulated Autophagy and Lysosome Function Are Linked to Exosome Production by Micro-RNA 155 in Alcoholic Liver Disease.Hepatology (Baltimore, Md.) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Autophagy is an important lysosome-mediated intracellular degradation pathway required for tissue homeostasis. Dysregulation of liver autophagy is closely associated with different liver diseases including alcoholic liver disease. Studies now indicate that autophagy may be induced or suppressed depending on the amount and the duration of ethanol treatment. Autophagy induced by ethanol serves as a protective mechanism, probably by selective degradation of the damaged mitochondria (mitophagy) and excess lipid droplets (lipophagy) and in turn attenuates alcohol-induced steatosis and liver injury. However, the detailed molecular mechanism of selective targeting of mitochondria and lipid is still unclear. Autophagy may possess other functions that protect hepatocytes from ethanol. Understanding these molecular entities would be essential in order to therapeutically module autophagy for treatment of alcoholic liver disease.
Indexed as
Identifiers
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.