ArticlePulmonary circulation
Skeletal muscle mitochondrial oxidative phosphorylation function in idiopathic pulmonary arterial hypertension: in vivo and in vitro study.
Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Evolution of Exercise Training in Patients with Pulmonary Hypertension-A Comprehensive Review.Healthcare (Basel, Switzerland) · 2026Review
- Beyond the Vasculature: The Emerging Role of Systemic Metabolism and Immunometabolism in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2026Review
- Bayesian classification of OXPHOS deficient skeletal myofibres.PLoS computational biology · 2025Article
- Multidimensional study on mitochondrial dysfunction in pulmonary hypertension.Frontiers in medicine · 2025Review
- Article
- Reduced exercise capacity occurs before intrinsic skeletal muscle dysfunction in experimental rat models of pulmonary hypertension.Pulmonary circulation · 2024Article
- Resistance Exercise Training Rescues Mitochondrial Dysfunction in Skeletal Muscle of Patients with Myotonic Dystrophy Type 1.Journal of neuromuscular diseases · 2023Article
- Bioinformatic analysis of dysregulated circular RNAs in pediatric pulmonary hypertension linked congenital heart disease.Translational pediatrics · 2022Article
- Skeletal muscle deficits are associated with worse exercise performance in pediatric pulmonary hypertension.Frontiers in pediatrics · 2022Article
- Exercise intolerance in pulmonary arterial hypertension: insight into central and peripheral pathophysiological mechanisms.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Skeletal and Respiratory Muscle Dysfunctions in Pulmonary Arterial Hypertension.Journal of clinical medicine · 2020Review
- Beyond the Lungs: Systemic Manifestations of Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2020Review
- Mitochondrial Dysfunction: Metabolic Drivers of Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Chemical exchange saturation transfer imaging of phosphocreatine in the muscle.Magnetic resonance in medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction within the pulmonary vessels has been shown to contribute to the pathology of idiopathic pulmonary arterial hypertension (IPAH). We investigated the hypothesis of whether impaired exercise capacity observed in IPAH patients is in part due to primary mitochondrial oxidative phosphorylation (OXPHOS) dysfunction in skeletal muscle. This could lead to potentially new avenues of treatment beyond targeting the pulmonary vessels. Nine clinically stable participants with IPAH underwent cardiopulmonary exercise testing, in vivo and in vitro assessment of mitochondrial function by
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What OpenQuestion holds
Registered trials
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.