ArticleScientific reports2019
Hyperoxia but not AOX expression mitigates pathological cardiac remodeling in a mouse model of inflammatory cardiomyopathy.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Mitochondrial electron transport chain is essential for acute inflammatory stress responses in mouse fibroblasts.Scientific reports · 2026Article
- Rescuing Ischemic Brain Injury by Rewiring Mitochondrial Electron Flow.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial respiration is necessary for CD8Nature immunology · 2025Article
- Mitochondria complex III-generated superoxide is essential for IL-10 secretion in macrophages.Science advances · 2025Article
- Alternative oxidase blunts pseudohypoxia and photoreceptor degeneration due to RPE mitochondrial dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Hyperbaric oxygen treatment reveals spatiotemporal OXPHOS plasticity in the porcine heart.PNAS nexus · 2024Article
- From Beach to the Bedside: Harnessing Mitochondrial Function in Human Diseases Using New Marine-Derived Strategies.International journal of molecular sciences · 2024Review
- Noncoupled Mitochondrial Respiration as Therapeutic Approach for the Treatment of Metabolic Diseases: Focus on Transgenic Animal Models.International journal of molecular sciences · 2023Review
- Alternative oxidase causes cell type- and tissue-specific responses in mutator mice.Life science alliance · 2023Article
- Knockout of the Complex III subunit Uqcrh causes bioenergetic impairment and cardiac contractile dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Article
- Spatial adjustment of bioenergetics, a possible determinant of contractile adaptation and development of contractile failure.Frontiers in molecular medicine · 2023Review
- Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation.Nature immunology · 2022Article
- Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive expression of the chemokine Mcp1 in mouse cardiomyocytes creates a model of inflammatory cardiomyopathy, with death from heart failure at age 7-8 months. A critical pathogenic role has previously been proposed for induced oxidative stress, involving NADPH oxidase activation. To test this idea, we exposed the mice to elevated oxygen levels. Against expectation, this prevented, rather than accelerated, the ultrastructural and functional signs of heart failure. This result suggests that the immune signaling initiated by Mcp1 leads instead to the inhibition of cellular oxygen usage, for which mitochondrial respiration is an obvious target. To address this hypothesis, we combined the Mcp1 model with xenotopic expression of the alternative oxidase (AOX), which provides a sink for electrons blocked from passage to oxygen via respiratory complexes III and IV. Ubiquitous AOX expression provided only a minor delay to cardiac functional deterioration and did not prevent the induction of markers of cardiac and metabolic remodeling considered a hallmark of the model. Moreover, cardiomyocyte-specific AOX expression resulted in exacerbation of Mcp1-induced heart failure, and failed to rescue a second cardiomyopathy model directly involving loss of cIV. Our findings imply that mitochondrial involvement in the pathology of inflammatory cardiomyopathy is multifaceted and complex.
Indexed as
Identifiers
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.