ArticleJournal of the American Heart Association2019
Ultrastructural Changes of the Right Ventricular Myocytes in Pulmonary Arterial Hypertension.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
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- Targeting TOMM40 and TOMM22 to Rescue Statin-Impaired Mitochondrial Function, Dynamics, and Mitophagy in Skeletal Myotubes.International journal of molecular sciences · 2025Article
- Right Heart Failure in Critical and Chronic Care: Current Concepts, Challenges and Mechanical Support Strategies.Medical sciences (Basel, Switzerland) · 2025Review
- Multi-Protective Effects of Petunidin-3-O-(International journal of molecular sciences · 2024Article
- Right ventricular diastolic adaptation to pressure overload in different rat strains.Physiological reports · 2024Article
- Targeting the redox system for cardiovascular regeneration in aging.Aging cell · 2023Review
- Mitochondrial Integrity Is Critical in Right Heart Failure Development.International journal of molecular sciences · 2023Review
- Mitochondrial dysfunction in human hypertrophic cardiomyopathy is linked to cardiomyocyte architecture disruption and corrected by improving NADH-driven mitochondrial respiration.European heart journal · 2023Article
- Elamipretide mitigates ischemia-reperfusion injury in a swine model of hemorrhagic shock.Scientific reports · 2023Article
- Acquired disorders of mitochondrial metabolism and dynamics in pulmonary arterial hypertension.Frontiers in cell and developmental biology · 2023Review
- MicroRNA-194 inhibits isoproterenol-induced chronic cardiac hypertrophy via targeting CnA/NFATc2 signaling in H9c2 cells.Annals of translational medicine · 2022Article
- Antioxidant Activity of Vitamin C against LPS-Induced Septic Cardiomyopathy by Down-Regulation of Oxidative Stress and Inflammation.Current issues in molecular biology · 2022Article
- Comparative analysis of right ventricular metabolic reprogramming in pre-clinical rat models of severe pulmonary hypertension-induced right ventricular failure.Frontiers in cardiovascular medicine · 2022Article
- Interaction between coxsackievirus B3 infection and α-synuclein in models of Parkinson's disease.PLoS pathogens · 2021Article
- Article
- Resveratrol Prevents Right Ventricle Dysfunction, Calcium Mishandling, and Energetic Failure via SIRT3 Stimulation in Pulmonary Arterial Hypertension.Oxidative medicine and cellular longevity · 2021Article
- Pathophysiology of Acute and Chronic Right Heart Failure.Cardiology clinics · 2020Review
- Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway.International journal of molecular sciences · 2020Article
- Antioxidant Regulation of Cell Reprogramming.Antioxidants (Basel, Switzerland) · 2019Review
- Transmission Electron Microscopy Study of Mitochondria in Aging Brain Synapses.Antioxidants (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Background Pulmonary arterial hypertension ( PAH ) is a serious disease without cure. Elevated pulmonary vascular resistance puts strain on the right ventricle ( RV ) and patients die of RV failure. Subjecting Sprague-Dawley rats to SU 5416 injection and hypoxia promotes severe PAH with pulmonary vascular lesions similar to human disease and has been well utilized to investigate pulmonary vascular pathology. However, despite exhibiting severe RV fibrosis, these rats do not die. Recently, subjecting Fischer ( CDF ) rats to the same treatment to promote PAH was found to result in mortality. Thus, the present study performed detailed morphological characterizations of Fischer rats with PAH . Methods and Results Rats were subjected to SU 5416 injection and hypoxia for 3 weeks, followed by maintenance in normoxia. More than 90% of animals died within 6 weeks of the SU 5416 injection. Necropsy revealed the accumulation of fluid in the chest cavity, right ventricular hypertrophy and dilatation, hepatomegaly, and other indications of congestive heart failure. Time course studies demonstrated the progressive thickening of pulmonary arteries with the formation of concentric lamellae and plexiform lesions as well as RV fibrosis in PAH rats. Transmission electron microscopy demonstrated the destruction of the myofilaments, T-tubules, and sarcoplasmic reticulum. RV mitochondrial damage and fission were found in Fischer rats, but not in Sprague-Dawley rats, with PAH . Conclusions These results suggest that the destruction of RV mitochondria plays a role in the mechanism of PAH -induced death. The SU 5416/hypoxia model in Fischer rats should be useful for further investigating the mechanism of RV failure and finding effective therapeutic agents to increase the survival of PAH patients.
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