ArticleHepatology communications2017
Disrupted ER-to-Golgi Trafficking Underlies Anti-HIV Drugs and Alcohol-Induced Cellular Stress and Hepatic Injury.
Article in Hepatology communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Effects of Ritonavir, Lopinavir, and Alcohol on ABC Transporters and Secretion of Bile Acid and Bilirubin in Senescent Hepatocytes.International journal of molecular sciences · 2026Article
- Hepatitis B virus, alcohol, and liver cancer.Frontiers in oncology · 2026Review
- Alcohol, Anti-HIV Drugs, and/or Hippuric Acid Deteriorate Cellular Stresses in Senescent Hepatocytes and Aging Murine Liver.Journal of addiction & prevention · 2025Article
- Emerging role of natural killer cells in non-AIDS comorbidities during suppressive antiretroviral therapy.Current opinion in HIV and AIDS · 2025Review
- Dolutegravir induces endoplasmic reticulum stress at the blood-brain barrier.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- GOLPH3 promotes endotoxemia-induced liver and kidney injury through Golgi stress-mediated apoptosis and inflammatory response.Cell death & disease · 2023Article
- Molecular Factors and Pathways of Hepatotoxicity Associated with HIV/SARS-CoV-2 Protease Inhibitors.International journal of molecular sciences · 2023Review
- Organelle-Specific Mechanisms in Crosstalk between Apoptosis and Ferroptosis.Oxidative medicine and cellular longevity · 2023Review
- Treatment Effects of Integrated TCM and Western Medicine Treatment Scheme on COVID-19: A Single-armed Clinical Trial.Clinical complementary medicine and pharmacology · 2021Article
- Iron status influences non-alcoholic fatty liver disease in obesity through the gut microbiome.Microbiome · 2021Article
- Acetaldehyde suppresses HBV-MHC class I complex presentation on hepatocytes via induction of ER stress and Golgi fragmentation.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Ritonavir and Lopinavir Suppress RCE1 and CAAX Rab Proteins Sensitizing the Liver to Organelle Stress and Injury.Hepatology communications · 2020Article
- Role of alcohol in pathogenesis of hepatitis B virus infection.World journal of gastroenterology · 2020Review
- Comparison of Lipid Profile, Liver Enzymes, Creatine Kinase and Lactate Dehydrogenase Among Type II Diabetes Mellitus Patients on Statin Therapy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Protective Effects of Facilitated Removal of Blood Alcohol and Acetaldehyde Against Liver Injury in Animal Models Fed Alcohol and Anti-HIV Drugs.Alcoholism, clinical and experimental research · 2019Article
- Liver as a target of human immunodeficiency virus infection.World journal of gastroenterology · 2018Review
- Dissecting the Role of Disturbed ER-Golgi Trafficking in Antivirals and Alcohol Abuse-Induced Pathogenesis of Liver Disorders.Journal of drug abuse · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) stress and unfolded protein response (UPR) are involved in anti-human immunodeficiency virus (HIV) drugs and alcohol-induced liver disease in a significant number of patients infected with HIV. However, the precise mechanism by which the drugs and alcohol cause ER stress remains elusive. We found that ritonavir-boosted lopinavir (RL) activated two canonical UPR branches without activation of the third canonical activating transcription factor 6 (ATF6) branch in either HepG2 cells or primary mouse hepatocytes. In the RL-treated cells, ATF6 localization in the Golgi apparatus required for its activation was reduced; this was followed by Golgi fragmentation and dislocation/redistribution of Golgi-resident enzymes. Severities of Golgi fragmentation induced by other anti-HIV drugs varied and were correlated with the ER stress response. In the liver of mice fed RL, alcohol feeding deteriorated the Golgi fragmentation, which was correlated with ER stress, elevated alanine aminotransferase, and liver steatosis. The Golgi stress response (GSR) markers GCP60 and HSP47 were increased in RL-treated liver cells, and knockdown of transcription factor for immunoglobulin heavy-chain enhancer 3 of the GSR by small interfering RNA worsened RL-induced cell death. Cotreatment of pharmacological agent H89 with RL inhibited the RL-induced Golgi enzyme dislocation and ER stress. Moreover, the coat protein complex II (COPII) complexes that mediate ER-to-Golgi trafficking accumulated in the RL-treated liver cells; this was not due to interference of RL with the initial assembly of the COPII complexes. RL also inhibited Golgi fragmentation and reassembly induced by short treatment and removal of brefeldin A.
conclusionOur study indicates that ER-to-Golgi trafficking is disrupted by anti-HIV drugs and/or alcohol, and this contributes to subsequent ER stress and hepatic injury.
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.