ArticleObesity (Silver Spring, Md.)2022
Hepatocyte-specific eNOS deletion impairs exercise-induced adaptations in hepatic mitochondrial function and autophagy.
Article in Obesity (Silver Spring, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Contradictory Effects on Hepatocytes in ASMD.International journal of molecular sciences · 2026Review
- The role of liver sinusoidal endothelial cells in metabolic dysfunction-associated steatotic liver diseases and liver cancer: mechanisms and potential therapies.Angiogenesis · 2025Review
- Vitamin DExperimental biology and medicine (Maywood, N.J.) · 2025Article
- Sexually dimorphic hepatic mitochondrial adaptations to exercise: a mini-review.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Review
- Selective breeding for physical inactivity produces cognitive deficitsFrontiers in aging neuroscience · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveEndothelial nitric oxide synthase (eNOS) is a potential mediator of exercise-induced hepatic mitochondrial adaptations.
methodsHere, male and female hepatocyte-specific eNOS knockout (eNOS
resultsEX resolved the exacerbated hepatic steatosis in eNOS
conclusionsCollectively, this study demonstrates for the first time, to the authors' knowledge, the requirement of eNOS in hepatocytes in the EX-induced increases in hepatic fatty acid oxidation in male mice. Deletion of eNOS in hepatocytes also appears to impair the energy-sensing ability of the cell and inhibit the activation of the autophagy initiating factor ULK1. These data uncover the important and novel role of hepatocyte eNOS in EX-induced hepatic mitochondrial adaptations.
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