ArticleNitric oxide : biology and chemistry2016
Endothelial AMPK activation induces mitochondrial biogenesis and stress adaptation via eNOS-dependent mTORC1 signaling.
Article in Nitric oxide : biology and chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
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- A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan.Frontiers in endocrinology · 2021Review
- Can Metformin Exert as an Active Drug on Endothelial Dysfunction in Diabetic Subjects?Biomedicines · 2020Review
- Inhibition of protein glycosylation is a novel pro-angiogenic strategy that acts via activation of stress pathways.Nature communications · 2020Article
- Endothelial cell CD36 deficiency prevents normal angiogenesis and vascular repair.American journal of translational research · 2020Article
- SIRT1-Mediated Protective Effect ofNutrients · 2019Article
- JNK and cardiometabolic dysfunction.Bioscience reports · 2019Review
- A769662 Inhibits Insulin-Stimulated Akt Activation in Human Macrovascular Endothelial Cells Independent of AMP-Activated Protein Kinase.International journal of molecular sciences · 2018Article
- Endothelial Cell Aging: How miRNAs Contribute?Journal of clinical medicine · 2018Review
- Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance.Oxidative medicine and cellular longevity · 2018Review
- Interplay between Oxidative Stress and Nutrient Sensing Signaling in the Developmental Origins of Cardiovascular Disease.International journal of molecular sciences · 2017Review
- Friend or Foe: Dietary Restriction and Its Protective Effects on Responses to Ionizing Radiation.Dose-response : a publication of International Hormesis SocietyReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Metabolic stress sensors like AMP-activated protein kinase (AMPK) are known to confer stress adaptation and promote longevity in lower organisms. This study demonstrates that activating the metabolic stress sensor AMP-activated protein kinase (AMPK) in endothelial cells helps maintain normal cellular function by promoting mitochondrial biogenesis and stress adaptation. To better define the mechanisms whereby AMPK promotes endothelial stress resistance, we used 5-aminoimidazole-4-carboxamide riboside (AICAR) to chronically activate AMPK and observed stimulation of mitochondrial biogenesis in wild type mouse endothelium, but not in endothelium from endothelial nitric oxide synthase knockout (eNOS-null) mice. Interestingly, AICAR-enhanced mitochondrial biogenesis was blocked by pretreatment with the mammalian target of rapamycin complex 1 (mTORC1) inhibitor, rapamycin. Further, AICAR stimulated mTORC1 as determined by phosphorylation of its known downstream effectors in wild type, but not eNOS-null, endothelial cells. Together these data indicate that eNOS is needed to couple AMPK activation to mTORC1 and thus promote mitochondrial biogenesis and stress adaptation in the endothelium. These data suggest a novel mechanism for mTORC1 activation that is significant for investigations in vascular dysfunction.
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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.