ArticleInternational journal of molecular sciences2020
Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Optical, Tomographic, and Mass Spectrometry Imaging Methods for Burn Wounds: Capabilities, Limitations, and Clinical Potential.Biomedicines · 2026Review
- Evolving Burn Care: The Transition from Life Preservation to Life Restoration-A Narrative Review.Journal of clinical medicine · 2026Review
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Protective Effect of Paeoniae Radix Alba Carbonisata on Hepatic Amyloidosis by Regulating Calcium Homeostasis.International journal of molecular sciences · 2026Article
- Comprehensive analysis of m6A modification in lipopolysaccharide-induced acute lung injury in mice.Molecular medicine (Cambridge, Mass.) · 2024Article
- PARP1 Inhibition and Effect on Burn Injury-Induced Inflammatory Response and Cardiac Function.Journal of the American College of Surgeons · 2023Article
- Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.International journal of molecular sciences · 2023Review
- The Expression ofJournal of immunology research · 2023Article
- Mitochondrial dysfunction and mitophagy: crucial players in burn trauma and wound healing.Burns & trauma · 2023Review
- Cytokine Pathways in Cardiac Dysfunction following Burn Injury and Changes in Genome Expression.Journal of personalized medicine · 2022Review
- Regulation of Key Immune-Related Genes in the Heart Following Burn Injury.Journal of personalized medicine · 2022Article
- Article
- The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats.Scientific reports · 2021Article
- Carotid smooth muscle contractility changes after severe burn.Scientific reports · 2021Article
- Synaptosomal Actin Dynamics in the Developmental Visual Cortex Regulate Behavioral Visual Acuity in Rats.Investigative ophthalmology & visual science · 2021Article
- Effect of Mitochondrial Antioxidant (Mito-TEMPO) on Burn-Induced Cardiac Dysfunction.Journal of the American College of Surgeons · 2021Article
- The Genetic Evidence of Burn-Induced Cardiac Mitochondrial Metabolism Dysfunction.Biomedicines · 2020Article
- Pathological Responses of Cardiac Mitochondria to Burn Trauma.International journal of molecular sciences · 2020Review
- Sildenafil Recovers Burn-Induced Cardiomyopathy.Cells · 2020Article
- Mechanisms of Action of a Herbal Formula Huangqi Guizhi Wuwu Tang for the Management of Post-Stroke Related Numbness and Weakness: A Computational Molecular Docking Study.Journal of evidence-based integrative medicineArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Burn-induced heart dysfunction is a key factor for patient mortality. However, the molecular mechanisms are not yet fully elucidated. This study sought to understand whether burn-induced heart dysfunction is associated with cardiac mitochondrial dysfunction and interruption of the PDE5A-cGMP-PKG pathway. Sixty percent total body surface area (TBSA) scald burned rats (±sildenafil) were used in this study. A transmission electron microscope (TEM), real-time qPCR, O2K-respirometer, and electron transport chain assays were used to characterized molecular function. Cardiac mitochondrial morphological shapes were disfigured with a decline in mitochondrial number, area, and size, resulting in deficiency of cardiac mitochondrial replication. Burn induced a decrease in all mitDNA encoded genes. State 3 oxygen consumption was significantly decreased. Mitochondrial complex I substrate-energized or complex II substrate-energized and both of respiratory control ratio (RCRs) were decreased after burn. All mitochondrial complex activity except complex II were decreased in the burn group, correlating with decreases in mitochondrial ATP and MnSOD activity. Sildenafil, a inhibitor of the PDE5A-cGMP-PKG pathway, preserved the mitochondrial structure, respiratory chain efficiency and energy status in cardiac tissue. Furthermore, sildenafil treatment significantly restored ADP-conjugated respiration in burned groups. In conclusion, cardiac mitochondrial damage contributes to burn-induced heart dysfunction via the PDE5A-cGMP-PKG pathway.
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Registered trials
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