ArticlePediatric research2017
Preventing permeability transition pore opening increases mitochondrial maturation, myocyte differentiation and cardiac function in the neonatal mouse heart.
Article in Pediatric research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Blocking mitochondrial cyclophilin D ameliorates TSH-impaired defensive barrier of artery.Redox biology · 2018Trial
- Inhibition of Cyclophilin D Rescues Cardiac Function and Bioenergetic Defects Caused by Neonatal Hypoxia.JACC. Basic to translational science · 2026Article
- A Case of Complete Functional Myocardial Regeneration in a Human Neonate.JACC. Case reports · 2025Article
- Whole genome transcriptomics reveal distinct atrial versus ventricular responses to neonatal hyperoxia.American journal of physiology. Heart and circulatory physiology · 2025Article
- The Role of Mitochondrial Permeability Transition in Bone Metabolism, Bone Healing, and Bone Diseases.Biomolecules · 2024Review
- Mitochondrial permeability transition dictates mitochondrial maturation upon switch in cellular identity of hematopoietic precursors.Communications biology · 2024Article
- Article
- Mitochondrial Volume Regulation and Swelling Mechanisms in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Review
- Role of the Mitochondrial Permeability Transition in Bone Metabolism and Aging.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Why Don't More Mitochondrial Diseases Exhibit Cardiomyopathy?Journal of cardiovascular development and disease · 2023Article
- Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023Review
- Microbiota affects mitochondria and immune cell infiltrations via alternative polyadenylation during postnatal heart development.Frontiers in cell and developmental biology · 2023Article
- Propofol toxicity in the developing mouse heart mitochondria.Pediatric research · 2022Article
- Mitochondrial ATP Synthase Tetramer Disassembly following Blood-Based or del Nido Cardioplegia during Neonatal Cardiac Surgery.The journal of extra-corporeal technology · 2022Article
- Article
- Molecular mechanisms and consequences of mitochondrial permeability transition.Nature reviews. Molecular cell biology · 2022Review
- Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes.Stem cell research & therapy · 2021Review
- Involvement of phosphatase and tensin homolog-induced putative kinase 1/Parkin-mediated autophagy in angiotensin II-induced cardiac hypertrophy in C57BL/6 mice.The Journal of international medical research · 2020Article
- Cyclophilin D, Somehow a Master Regulator of Mitochondrial Function.Biomolecules · 2018Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn embryonic myocytes, closure of the mitochondrial permeability transition pore (PTP) drives mitochondrial maturation and cardiac myocyte differentiation. Since neonatal cardiac myocytes remain relatively immature, we hypothesized that inducing PTP closure at this age, by inhibiting the PTP regulator, cyclophilin D (CyPD), genetically or with Cyclosporin A (CsA) and NIM811, would increase cardiac function by increasing mitochondrial maturation and myocyte differentiation.
methodsCultured neonatal myocytes or neonatal mice were treated for 5 d with vehicle, CsA or NIM811. Mitochondrial function and structure were measured in vitro. Myocyte differentiation was assessed by immunolabeling for contractile proteins. Cardiac function was determined using echocardiography.
resultsThe probability of PTP opening was high in WT neonatal myocytes. Treatment with CsA or NIM811 in vitro increased mitochondrial structural complexity and membrane potential, decreased reactive oxygen species levels, and increased myocyte differentiation. WT mice treated with either CsA or NIM811 in vivo for the first 5 d of life had higher ejection fractions. Deleting CyPD had similar effects as CsA and NIM811 on all parameters.
conclusionsIt may be feasible to inhibit the PTP using available drugs to increase mitochondrial maturation, myocyte differentiation, and cardiac function in neonates.
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Registered trials
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