ArticleAmerican journal of physiology. Endocrinology and metabolism2019
eNOS deletion impairs mitochondrial quality control and exacerbates Western diet-induced NASH.
Article in American journal of physiology. Endocrinology and metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Endurance exercise elicits temporal and sexual dimorphic multi-omics remodeling of liver metabolism revealed by MoTrPAC.Cell reports · 2026Article
- Contradictory Effects on Hepatocytes in ASMD.International journal of molecular sciences · 2026Review
- Superoxide signals for the mitophagy of dysfunctional mitochondria to maintain quality control.Redox biology · 2026Review
- Novel therapeutic strategies targeting mitochondrial quality control for metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2026Review
- Loss of hepatocyte-specific RECK exacerbates metabolic dysfunction-associated steatohepatitis.American journal of physiology. Endocrinology and metabolism · 2025Article
- Loss of ovarian function prevents exercise-induced activation of hepatic mitophagic flux.American journal of physiology. Endocrinology and metabolism · 2025Article
- Mitochondria at the Crossroads: Linking the Mediterranean Diet to Metabolic Health and Non-Pharmacological Approaches to NAFLD.Nutrients · 2025Review
- Impact and Mechanisms of Action of BDNF on Neurological Disorders, Cancer, and Cardiovascular Diseases.CNS neuroscience & therapeutics · 2024Review
- Gut microbial metabolites in MASLD: Implications of mitochondrial dysfunction in the pathogenesis and treatment.Hepatology communications · 2024Review
- Liver Cell Mitophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease and Liver Fibrosis.Antioxidants (Basel, Switzerland) · 2024Review
- Chronic kidney disease and left ventricular diastolic dysfunction (CKD-LVDD) alter cardiac expression of mitochondria-related genes in swine.Translational research : the journal of laboratory and clinical medicine · 2024Article
- The crosstalk between mitochondrial quality control and metal-dependent cell death.Cell death & disease · 2024Review
- Relationship between serum β-hydroxybutyrate and hepatic fatty acid oxidation in individuals with obesity and NAFLD.American journal of physiology. Endocrinology and metabolism · 2024Article
- Dysfunction of autophagy in high-fat diet-induced non-alcoholic fatty liver disease.Autophagy · 2024Review
- Mitophagy in fibrotic diseases: molecular mechanisms and therapeutic applications.Frontiers in physiology · 2024Review
- Cell-type specific role of autophagy in the liver and its implications in non-alcoholic fatty liver disease.World journal of hepatology · 2023Article
- Review
- Mitochondrial metabolic dysfunction and non-alcoholic fatty liver disease: new insights from pathogenic mechanisms to clinically targeted therapy.Journal of translational medicine · 2023Review
- Review
- Hepatic Mitochondria-Gut Microbiota Interactions in Metabolism-Associated Fatty Liver Disease.Metabolites · 2023Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Dysregulated mitochondrial quality control leads to mitochondrial functional impairments that are central to the development and progression of hepatic steatosis to nonalcoholic steatohepatitis (NASH). Here, we identify hepatocellular localized endothelial nitric oxide synthase (eNOS) as a novel master regulator of mitochondrial quality control. Mice lacking eNOS were more susceptible to Western diet-induced hepatic inflammation and fibrosis in conjunction with decreased markers of mitochondrial biogenesis and turnover. The hepatocyte-specific influence was verified via magnetic activated cell sorting purified primary hepatocytes and in vitro siRNA-induced knockdown of eNOS. Hepatic mitochondria from eNOS knockout mice revealed decreased markers of mitochondrial biogenesis (PPARγ coactivator-1α, mitochondrial transcription factor A) and autophagy/mitophagy [BCL-2-interacting protein-3 (BNIP3), 1A/1B light chain 3B (LC3)], suggesting decreased mitochondrial turnover rate. eNOS knockout in primary hepatocytes exhibited reduced fatty acid oxidation capacity and were unable to mount a normal BNIP3 response to a mitophagic challenge compared with wild-type mice. Finally, we demonstrate that eNOS is required in primary hepatocytes to induce activation of the stress-responsive transcription factor nuclear factor erythroid 2-related factor 2 (
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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.