ArticleInternational journal of molecular sciences2023
Malonyl-CoA Accumulation as a Compensatory Cytoprotective Mechanism in Cardiac Cells in Response to 7-Ketocholesterol-Induced Growth Retardation.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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
6 citing papers in PubMed.
- Malonyl-CoA Decarboxylase: A Spotlight on Brain Aspects.Brain sciences · 2026Review
- NRF2-SOX4 complex regulates PSPH in hepatocellular carcinoma and modulates M2 macrophage differentiation.Cancer gene therapy · 2025Article
- Downregulation of NAD Kinase Expression in β-Cells Contributes to the Aging-Associated Decline in Glucose-Stimulated Insulin Secretion.Aging cell · 2025Article
- Carvedilol Confers Ferroptosis Resistance in HL-1 Cells by Upregulating GPX4, FTH1, and FTL1 and Inducing Metabolic Remodeling Under Hypoxia/Reoxygenation.Antioxidants (Basel, Switzerland) · 2024Article
- Molecular Mechanisms of Cardiac Development and Disease.International journal of molecular sciences · 2023Article
- Case report: A novel 5'-UTR-exon1-intron1 deletion in MLYCD in an IVF child with malonyl coenzyme A decarboxylase deficiency and literature review.Frontiers in medicine · 2023Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The major oxidized product of cholesterol, 7-Ketocholesterol (7KCh), causes cellular oxidative damage. In the present study, we investigated the physiological responses of cardiomyocytes to 7KCh. A 7KCh treatment inhibited the growth of cardiac cells and their mitochondrial oxygen consumption. It was accompanied by a compensatory increase in mitochondrial mass and adaptive metabolic remodeling. The application of [U-
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Registered trials
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