ArticleRedox biology2015
Complex I dysfunction underlies the glycolytic switch in pulmonary hypertensive smooth muscle cells.
Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 100 citations in OpenAlex.
- Hypoxia rescues complex 1-associated disease caused by proteostatic defects.Nature metabolism · 2026Article
- Malonic acid promotes glycolytic activity in cumulus cells and improves the quality of bovine oocytes matured in vitro.The Journal of reproduction and development · 2026Article
- Pulmonary arterial hypertension from a translational perspective: Bridging pathophysiology and treatment.Chinese medical journal · 2026Review
- miR-423-5p/NDUFS7-mediated mitochondrial function modulation contributes to quercetin-induced attenuation of pulmonary fibrosis via extracellular matrix remodeling regulation.Non-coding RNA research · 2026Article
- Mitochondrial dysfunction triggers a maladaptive peroxisomal response driving lipid accumulation.Redox biology · 2026Article
- Prenatal glucocorticoid exposure programs long-term left ventricular metabolism, function, and remodeling in baboons.American journal of physiology. Heart and circulatory physiology · 2026Article
- Lactate: elucidating its indispensable role in human health.Molecular cancer · 2026Review
- BK channels are indispensable for endothelial function in small pulmonary arteries.Cell communication and signaling : CCS · 2025Article
- Biventricular electromechanical dysfunction and molecular remodeling in a rat model of advanced pulmonary arterial hypertension.Journal of translational medicine · 2025Article
- Stroke in Pregnancy Brings Epigenetic Changes in Correlation with Affected Mitochondrial Dynamics and Inflammasome Mediated Apoptosis in Rodents.Journal of the American Heart Association · 2025Article
- Restoration of pp60International journal of molecular sciences · 2025Article
- Exploration of the metabolomic mechanisms of postmenopausal hypertension induced by low estrogen state.eLife · 2025Article
- Multidimensional study on mitochondrial dysfunction in pulmonary hypertension.Frontiers in medicine · 2025Review
- Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies.The journal of cardiovascular aging · 2025Article
- Mitochondria as a primary determinant of angiogenic modality in pulmonary arterial hypertension.The Journal of experimental medicine · 2024Article
- Metabolic Responses to Redox Stress in Vascular Cells.Antioxidants & redox signaling · 2024Review
- The mitochondrial redistribution of ENOS is regulated by AKT1 and dimer status.Nitric oxide : biology and chemistry · 2024Article
- Lactylation: An Innovative Approach to Disease Control.Aging and disease · 2024Review
- Mitochondrial hyperfusion induces metabolic remodeling in lung endothelial cells by modifying the activities of electron transport chain complexes I and III.Free radical biology & medicine · 2024Article
- Transcriptional profiles of pulmonary artery endothelial cells in pulmonary hypertension.Scientific reports · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
ATP is essential for cellular function and is usually produced through oxidative phosphorylation. However, mitochondrial dysfunction is now being recognized as an important contributing factor in the development cardiovascular diseases, such as pulmonary hypertension (PH). In PH there is a metabolic change from oxidative phosphorylation to mainly glycolysis for energy production. However, the mechanisms underlying this glycolytic switch are only poorly understood. In particular the role of the respiratory Complexes in the mitochondrial dysfunction associated with PH is unresolved and was the focus of our investigations. We report that smooth muscle cells isolated from the pulmonary vessels of rats with PH (PH-PASMC), induced by a single injection of monocrotaline, have attenuated mitochondrial function and enhanced glycolysis. Further, utilizing a novel live cell assay, we were able to demonstrate that the mitochondrial dysfunction in PH-PASMC correlates with deficiencies in the activities of Complexes I-III. Further, we observed that there was an increase in mitochondrial reactive oxygen species generation and mitochondrial membrane potential in the PASMC isolated from rats with PH. We further found that the defect in Complex I activity was due to a loss of Complex I assembly, although the assembly of Complexes II and III were both maintained. Thus, we conclude that loss of Complex I assembly may be involved in the switch of energy metabolism in smooth muscle cells to glycolysis and that maintaining Complex I activity may be a potential therapeutic target for the treatment of PH.
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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.