ArticleFree radical biology & medicine2024
Mitochondrial hyperfusion induces metabolic remodeling in lung endothelial cells by modifying the activities of electron transport chain complexes I and III.
Article in Free radical biology & medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Mitochondrial acid-sensing ion channel 1a deficiency induces mitochondrial dysfunction in pulmonary arterial smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Rewriting the vascular script: epigenetic modifiers as scribes of metabolic reprogramming in pulmonary hypertension.Journal of molecular medicine (Berlin, Germany) · 2025Review
- c-Myc promotes metabolic reprogramming in pulmonary hypertension via the stimulation of glutaminolysis and the reductive tricarboxylic acid cycle.Redox biology · 2025Article
- Critical role of mitochondrial dynamics in chronic respiratory diseases and new therapeutic directions.Chinese medical journal · 2025Review
- Metabolic Disturbances Involved in Cardiovascular Diseases: The Role of Mitochondrial Dysfunction, Altered Bioenergetics and Oxidative Stress.International journal of molecular sciences · 2025Review
- Review on the Role of Mitochondrial Dysfunction in Septic Encephalopathy.Cell biochemistry and biophysics · 2025Review
- Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.Frontiers in pharmacology · 2025Review
- Interaction of ferroptosis and cuproptosis in the perspective of pulmonary hypertension.Frontiers in cardiovascular medicine · 2025Review
- Emerging role of the TCA cycle and its metabolites in lung disease.Frontiers in physiology · 2025Review
- Peroxisome proliferator-activated receptors-mediated diabetic wound healing regulates endothelial cells' mitochondrial function via sonic hedgehog signaling.Burns & trauma · 2025Article
- Effects of sodium-glucose cotransport-2 inhibitors treatment in patients with pulmonary hypertension.Therapeutic advances in respiratory diseaseArticle
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
objectivePulmonary hypertension (PH) is a progressive disease with vascular remodeling as a critical structural alteration. We have previously shown that metabolic reprogramming is an early initiating mechanism in animal models of PH. This metabolic dysregulation has been linked to remodeling the mitochondrial network to favor fission. However, whether the mitochondrial fission/fusion balance underlies the metabolic reprogramming found early in PH development is unknown.
methodsUtilizing a rat early model of PH, in conjunction with cultured pulmonary endothelial cells (PECs), we utilized metabolic flux assays, Seahorse Bioassays, measurements of electron transport chain (ETC) complex activity, fluorescent microscopy, and molecular approaches to investigate the link between the disruption of mitochondrial dynamics and the early metabolic changes that occur in PH.
resultsWe observed increased fusion mediators, including Mfn1, Mfn2, and Opa1, and unchanged fission mediators, including Drp1 and Fis1, in a two-week monocrotaline-induced PH animal model (early-stage PH). We were able to establish a connection between increases in fusion mediator Mfn1 and metabolic reprogramming. Using an adenoviral expression system to enhance Mfn1 levels in pulmonary endothelial cells and utilizing
conclusionsOur data connects mitochondrial fusion-mediated mt-ROS to the Warburg phenotype in early-stage PH development.
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