ArticleJournal of molecular and cellular cardiology plus2025
Mitochondrial metabolic remodeling and multi-omics profiling identify plasma biomarkers of myocardial infarction.
Article in Journal of molecular and cellular cardiology plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Understanding Pathophysiological Complexity of Feline Hypertrophic Cardiomyopathy Using SWATH-MS Plasma Proteomics.Animals : an open access journal from MDPI · 2026Article
- Single-cell RNA sequencing and integrated bioinformatics reveal new mitochondrial biomarkers in sarcopenia.Frontiers in molecular biosciences · 2026Article
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is a hallmark of myocardial infarction (MI), yet the molecular mechanisms linking metabolic reprogramming in the ischemic myocardium to systemic biomarker signatures remain incompletely understood. In this study, we employed a data-independent acquisition mass spectrometry (SWATH-MS) strategy integrating multi-omics analysis with upstream regulatory network analysis to investigate mitochondrial energy pathway alterations in a preclinical ovine model of MI. Proteomic profiling of infarcted myocardium revealed a pronounced shift from oxidative phosphorylation to glycolysis, accompanied by coordinated suppression of mitochondrial fatty acid β-oxidation enzymes. This metabolic reprogramming was strongly associated with four upstream master regulators, most notably predicted inhibition and significant transcriptional downregulation of
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