ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Mitochondrial integrity in a neonatal bovine model of right ventricular dysfunction.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.
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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
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.
- Metabolic Remodeling in the Pressure-Loaded Right Ventricle: Shifts in Glucose and Fatty Acid Metabolism-A Systematic Review and Meta-Analysis.Journal of the American Heart Association · 2019Pooled it
- Assessment of Right Ventricular Function in the Research Setting: Knowledge Gaps and Pathways Forward. An Official American Thoracic Society Research Statement.American journal of respiratory and critical care medicine · 2018Guideline
- Functional and molecular determinants of right ventricular response to severe pulmonary hypertension in a large animal model.American journal of physiology. Heart and circulatory physiology · 2023Article
- PGC-1α activity and mitochondrial dysfunction in preterm infants.Frontiers in physiology · 2022Review
- Resveratrol Prevents Right Ventricle Dysfunction, Calcium Mishandling, and Energetic Failure via SIRT3 Stimulation in Pulmonary Arterial Hypertension.Oxidative medicine and cellular longevity · 2021Article
- Band on the run: insights into right ventricular reverse remodelling.Cardiovascular research · 2020Article
- Characterizing the impact of altitude and finishing system on mean pulmonary arterial pressure and carcass characteristics in Angus cattle.Translational animal science · 2019Article
- Metabolic Response to Stress by the Immature Right Ventricle Exposed to Chronic Pressure Overload.Journal of the American Heart Association · 2019Article
- Metabolic Reprogramming in the Heart and Lung in a Murine Model of Pulmonary Arterial Hypertension.Frontiers in cardiovascular medicine · 2018Article
- Novel putative pharmacological therapies to protect the right ventricle in pulmonary hypertension: a review of current literature.British journal of pharmacology · 2017Review
- Update on novel targets and potential treatment avenues in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Mitochondrial fusion and fission proteins as novel therapeutic targets for treating cardiovascular disease.European journal of pharmacology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Right ventricular (RV) function is a key determinant of survival in patients with both RV and left ventricular (LV) failure, yet the mechanisms of RV failure are poorly understood. Recent studies suggest cardiac metabolism is altered in RV failure in pulmonary hypertension (PH). Accordingly, we assessed mitochondrial content, dynamics, and function in hearts from neonatal calves exposed to hypobaric hypoxia (HH). This model develops severe PH with concomitant RV hypertrophy, dilation, and dysfunction. After 2 wk of HH, pieces of RV and LV were obtained along with samples from age-matched controls. Comparison with control assesses the effect of hypoxia, whereas comparison between the LV and RV in HH assesses the additional impact of RV overload. Mitochondrial DNA was unchanged in HH, as was mitochondrial content as assessed by electron microscopy. Immunoblotting for electron transport chain subunits revealed a small increase in mitochondrial content in HH in both ventricles. Mitochondrial dynamics were largely unchanged. Activity of individual respiratory chain complexes was reduced (complex I) or unchanged (complex V) in HH. Key enzymes in the glycolysis pathway were upregulated in both HH ventricles, alongside upregulation of hypoxia-inducible factor-1α protein. Importantly, none of the changes in expression or activity were different between ventricles, suggesting the changes are in response to HH and not RV overload. Upregulation of glycolytic modulators without chamber-specific mitochondrial dysfunction suggests that mitochondrial capacity and activity are maintained at the onset of PH, and the early RV dysfunction in this model results from mechanisms independent of the mitochondria.
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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.