ArticleThe Journal of biological chemistry2020
ERAD deficiency promotes mitochondrial dysfunction and transcriptional rewiring in human hepatic cells.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Huangjing Jiangzhi Granules Ameliorate Nonalcoholic Fatty Liver Disease by Activating the FOXA1-DERL1 Regulatory Axis to Suppress Lipid Accumulation, Endoplasmic Reticulum Stress, and Apoptosis.Biological procedures online · 2026Article
- Protein quality control and antigen presentation in the development of hepatitis B-related hepatocellular carcinoma.Frontiers in pharmacology · 2026Review
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- Ubiquitin regulatory X (UBX) domain-containing protein 6 is essential for autophagy induction and inflammation control in macrophages.Cellular & molecular immunology · 2024Article
- Roles of ubiquitin‑specific protease 13 in normal physiology and tumors (Review).Oncology letters · 2024Review
- Establishment of aJournal of pathogens · 2024Article
- SEL1L preserves CD8Cellular & molecular immunology · 2023Article
- Role of CELF2 in ferroptosis: Potential targets for cancer therapy (Review).International journal of molecular medicine · 2023Review
- Association between SYVN1 and SEL1 genetic polymorphisms and remission in rheumatoid arthritis patients treated with TNF-α inhibitors: a machine learning approach.Immunologic research · 2023Article
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- SMURF1 attenuates endoplasmic reticulum stress by promoting the degradation of KEAP1 to activate NRF2 antioxidant pathway.Cell death & disease · 2023Article
- Estimation of Metabolic Effects upon Cadmium Exposure during Pregnancy Using Tensor Decomposition.Genes · 2022Article
- Endoplasmic reticulum-unfolded protein response pathway modulates the cellular response to mitochondrial proteotoxic stress.Cell stress & chaperones · 2022Article
- ER Disposal Pathways in Chronic Liver Disease: Protective, Pathogenic, and Potential Therapeutic Targets.Frontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is associated with a variety of human diseases including neurodegeneration, diabetes, nonalcohol fatty liver disease (NAFLD), and cancer, but its underlying causes are incompletely understood. Using the human hepatic cell line HepG2 as a model, we show here that endoplasmic reticulum-associated degradation (ERAD), an ER protein quality control process, is critically required for mitochondrial function in mammalian cells. Pharmacological inhibition or genetic ablation of key proteins involved in ERAD increased cell death under both basal conditions and in response to proinflammatory cytokines, a situation frequently found in NAFLD. Decreased viability of ERAD-deficient HepG2 cells was traced to impaired mitochondrial functions including reduced ATP production, enhanced reactive oxygen species (ROS) accumulation, and increased mitochondrial outer membrane permeability. Transcriptome profiling revealed widespread down-regulation of genes underpinning mitochondrial functions, and up-regulation of genes associated with tumor growth and aggression. These results highlight a critical role for ERAD in maintaining mitochondrial functional and structural integrity and raise the possibility of improving cellular and organismal mitochondrial function via enhancing cellular ERAD capacity.
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