ArticleThe Biochemical journal2002
Endothelial nitric oxide synthase (NOS) deficiency affects energy metabolism pattern in murine oxidative skeletal muscle.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 43 citations in OpenAlex.
- The Endothelium as a Central Mediator of Exercise-Induced Metabolism and Communication.Exercise and sport sciences reviews · 2026Review
- Endothelial Reactive Oxygen Species: Key Players in Cardiovascular Health and Disease.Antioxidants & redox signaling · 2025Review
- Type 2 diabetes-related sarcopenia: role of nitric oxide.Nutrition & metabolism · 2024Review
- Metabolism in Pulmonary Hypertension.Annual review of physiology · 2021Review
- Endothelial nitric oxide synthase-derived nitric oxide in the regulation of metabolism.F1000Research · 2020Review
- Activated whole-body arginine pathway in high-active mice.PloS one · 2020Article
- Oral nitrite restores age-dependent phenotypes in eNOS-null mice.JCI insight · 2018Article
- Hemoglobin: a nitric-oxide dioxygenase.Scientifica · 2012Review
- Endothelial cell energy metabolism, proliferation, and apoptosis in pulmonary hypertension.Comprehensive Physiology · 2011Review
- Low creatine kinase is associated with a high population incidence of fainting.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2009Article
- Really different knockout strains in movement?The Journal of physiology · 2008Article
- Mitochondrial pathophysiology, reactive oxygen species, and cardiovascular diseases.The Veterinary clinics of North America. Small animal practice · 2008Review
- NOS isoform-specific regulation of basal but not exercise-induced mitochondrial biogenesis in mouse skeletal muscle.The Journal of physiology · 2007Article
- Alterations of cellular bioenergetics in pulmonary artery endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Mitochondrial biogenesis by NO yields functionally active mitochondria in mammals.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative capacity of muscles correlates with capillary density and with microcirculation, which in turn depend on various regulatory factors, including NO generated by endothelial nitric oxide synthase (eNOS). To determine the role of eNOS in patterns of regulation of energy metabolism in various muscles, we studied mitochondrial respiration in situ in saponin-permeabilized fibres as well as the energy metabolism enzyme profile in the cardiac, soleus (oxidative) and gastrocnemius (glycolytic) muscles isolated from mice lacking eNOS (eNOS(-/-)). In soleus muscle, the absence of eNOS induced a marked decrease in both basal mitochondrial respiration without ADP (-32%; P <0.05) and maximal respiration in the presence of ADP (-29%; P <0.05). Furthermore, the eNOS(-/-) soleus muscle showed a decrease in total creatine kinase (-29%; P <0.05), citrate synthase (-31%; P <0.01), adenylate kinase (-27%; P <0.05), glyceraldehyde-3-phosphate dehydrogenase (-43%; P <0.01) and pyruvate kinase (-26%; P <0.05) activities. The percentage of myosin heavy chains I (slow isoform) was significantly increased from 24.3+/-1.5% in control to 30.1+/-1.1% in eNOS(-/-) soleus muscle ( P <0.05) at the expense of a slight non-significant decrease in the three other (fast) isoforms. Besides, eNOS(-/-) soleus showed a 28% loss of weight. Interestingly, we did not find differences in any parameters in cardiac and gastrocnemius muscles compared with respective controls. These results show that eNOS knockout has an important effect on muscle oxidative capacity as well on the activities of energy metabolism enzymes in oxidative (soleus) muscle. The absence of such effects in cardiac and glycolytic (gastrocnemius) muscle suggests a specific role for eNOS-produced NO in oxidative skeletal muscle.
Indexed as
Identifiers
What OpenQuestion holds
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.