ArticleRedox biology2017
Autophagy regulates turnover of lipid droplets via ROS-dependent Rab25 activation in hepatic stellate cell.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 54 papers, 1 of them a synthesis that pooled it.
What it found
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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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Research trends of mitochondrial dysfunction in hepatic fibrosis: a bibliometric analysis.Frontiers in physiology · 2026Pooled it
- LncRNA H19 as a key regulator in biliary atresia: insights into pathogenesis and potential therapeutic targets.Annals of medicine · 2026Review
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- Reduced Esterification Rather Than Increased Hydrolysis Is Causative for Loss of Hepatic Retinoids Upon CClLiver international : official journal of the International Association for the Study of the Liver · 2025Article
- Diallyl Trisulfide From Garlic Regulates RAB18 Phase Separation to Inhibit Lipophagy and Induce Cuproptosis in Hepatic Stellate Cells for Antifibrotic Effects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Metabolic Sparks in the Liver: Metabolic and Epigenetic Reprogramming in Hepatic Stellate Cells Activation and Its Implications for Human Metabolic Diseases.Diabetes & metabolism journal · 2025Review
- Article
- Acetoacetate Ameliorates Hepatic Fibrosis by Targeting Peroxisome Proliferator-Activated Receptor Gamma to Restore Lipid Droplets in Activated Hepatic Stellate Cells.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Ginsenoside Rd protects against acute liver injury by regulating the autophagy NLRP3 inflammasome pathway.Scientific reports · 2025Article
- Real-Time Visualization of Cholesterol Trafficking in Human Granulosa Cells Using Confocal Live Cell Microscopy as a Tool to Study the Novel Role of Autophagy in Sex Steroid Synthesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Fangchinoline attenuates hepatic fibrosis by regulating taurine metabolism and oxidative stress.Frontiers in pharmacology · 2025Article
- Lipids associated with autophagy: mechanisms and therapeutic targets.Cell death discovery · 2024Review
- Novel AT2 Cell Subpopulations and Diagnostic Biomarkers in IPF: Integrating Machine Learning with Single-Cell Analysis.International journal of molecular sciences · 2024Article
- The cell fate regulator DACH1 modulates ferroptosis through affecting P53/SLC25A37 signaling in fibrotic disease.Hepatology communications · 2024Article
- Identification of potential biomarkers from amino acid transporter in the activation of hepatic stellate cells via bioinformatics.Frontiers in genetics · 2024Article
- Advances in the pharmacological mechanisms of berberine in the treatment of fibrosis.Frontiers in pharmacology · 2024Review
- Emerging role of lipophagy in liver disorders.Molecular and cellular biochemistry · 2024Review
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Lipid droplets: a cellular organelle vital in cancer cells.Cell death discovery · 2023Review
Corrections and comments
- Retracted
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of hepatic stellate cells (HSCs) is a pivotal event in liver fibrosis, characterized by dramatic disappearance of lipid droplets (LDs). Although LD disappearance has long been considered one of the hallmarks of HSC activation, the underlying molecular mechanisms are largely unknown. In this study, we sought to investigate the role of autophagy in the process of LD disappearance, and to further examine the underlying mechanisms in this molecular context. We found that LD disappearance during HSC activation was associated with a coordinate increase in autophagy. Inhibition or depletion of autophagy by Atg5 siRNA impaired LD disappearance of quiescent HSCs, and also restored lipocyte phenotype of activated HSCs. In contrast, induction of autophagy by Atg5 plasmid accelerated LD loss of quiescent HSCs. Importantly, our study also identified a crucial role for reactive oxygen species (ROS) in the facilitation of autophagy activation. Antioxidants, such as glutathione and N-acetyl cysteine, significantly abrogated ROS production, and in turn, prevented autophagosome generation and autophagic flux during HSC activation. Besides, we found that HSC activation triggered Rab25 overexpression, and promoted the combination of Rab25 and PI3KCIII, which direct autophagy to recognize, wrap and degrade LDs. Down-regulation of Rab25 activity, using Rab25 siRNA, blocked the target recognition of autophagy on LDs, and inhibited LD disappearance of quiescent HSCs. Moreover, the scavenging of excessive ROS could disrupt the interaction between autophagy and Rab25, and increase intracellular lipid content. Overall, these results provide novel implications to reveal the molecular mechanism of LD disappearance during HSC activation, and also identify ROS-Rab25-dependent autophagy as a potential target for the treatment of liver fibrosis.
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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.