ReviewThe American journal of pathology2023
The Role of Endoplasmic Reticulum in Lipotoxicity during Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Pathogenesis.
Review in The American journal of pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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
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Who cites it
47 citing papers in PubMed, 55 citations in OpenAlex.
- Lipid Metabolic Reprogramming and Bioactive Lipid Signaling in MASLD: Molecular Mechanisms, Pathogenesis and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Imeglimin-Associated Temporal Changes in γ-Glutamyl Transferase and Total Cholesterol: A Post Hoc Exploratory Analysis of the INFINITY Study.Journal of personalized medicine · 2026Article
- Jiuwei Xiaozhi Decoction Alleviates High-Fat Diet-Induced MASLD by Suppressing Hepatic SREBP2-Driven Cholesterogenesis and Restoring PPARα-Mediated Fatty Acid Oxidation.Chemical biology & drug design · 2026Article
- Quercetin alleviates endoplasmic reticulum stress and apoptosis through activation of g protein-coupled estrogen receptor signaling in laying hens with fatty liver hemorrhagic syndrome.Poultry science · 2026Article
- Mitochondrial Dysfunction in Metabolic-Syndrome-Related MASLD/MASH: Metabolic Mechanisms and Therapeutic Perspectives.Metabolites · 2026Review
- Oxidative Stress Biomarkers and Systemic Inflammatory Indices in Metabolic Dysfunction-Associated Steatotic Liver Disease with Type 2 Diabetes Mellitus: A Comparative and Longitudinal Analysis.International journal of molecular sciences · 2026Observational
- Integrating CRISPR genome editing with liver organoid and hiPSC-derived microfluidic platforms to model metabolic dysfunction-associated steatotic liver disease.Biochemistry and biophysics reports · 2026Review
- Fucoxanthin Ameliorates MASLD by Directly Targeting GRP78 to Restore ER Homeostasis and Activate AMPK Signaling.Food science & nutrition · 2026Article
- Metabolic Dysfunction-Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach.The Kaohsiung journal of medical sciences · 2026Review
- Role of Sirtuin 6 in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Current issues in molecular biology · 2026Review
- ABCA12 and stress: a molecular insight into lipid transport and cellular resilience.Psychopharmacology · 2026Review
- Burden and Health System Challenges in MASLD Across East and Southeast Asia: A Narrative Review.Health science reports · 2026Review
- MASLD biomarker discovery: evaluating lipidomics techniques across disease progression.Molecular biology reports · 2026Review
- Lysophosphatidylethanolamine Degradation Associated with Upregulation of Pnpla6/7 in a Murine Model of Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and type 2 diabetes: Pathophysiology, diagnosis, and emerging therapeutic strategies.World journal of diabetes · 2026Review
- Article
- Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk.Lipids in health and disease · 2026Review
- Article
- Hepatic loss of AATF attenuates MASH by suppressing AKT-mTORC1 signaling and reprogramming lipid metabolism.Molecular medicine (Cambridge, Mass.) · 2026Article
- Ferroptosis in metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Perturbations in lipid and protein homeostasis induce endoplasmic reticulum (ER) stress in metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease. Lipotoxic and proteotoxic stress can activate the unfolded protein response (UPR) transducers: inositol requiring enzyme1α, PKR-like ER kinase, and activating transcription factor 6α. Collectively, these pathways induce expression of genes that encode functions to resolve the protein folding defect and ER stress by increasing the protein folding capacity of the ER and degradation of misfolded proteins. The ER is also intimately connected with lipid metabolism, including de novo ceramide synthesis, phospholipid and cholesterol synthesis, and lipid droplet formation. Following their activation, the UPR transducers also regulate lipogenic pathways in the liver. With persistent ER stress, cellular adaptation fails, resulting in hepatocyte apoptosis, a pathological marker of liver disease. In addition to the ER-nucleus signaling activated by the UPR, the ER can interact with other organelles via membrane contact sites. Modulating intracellular communication between ER and endosomes, lipid droplets, and mitochondria to restore ER homeostasis could have therapeutic efficacy in ameliorating liver disease. Recent studies have also demonstrated that cells can convey ER stress by the release of extracellular vesicles. This review discusses lipotoxic ER stress and the central role of the ER in communicating ER stress to other intracellular organelles in MASLD pathogenesis.
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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.