ArticleJournal of cellular and molecular medicine2024
Cardiomyocyte-specific overexpression of FPN1 diminishes cardiac hypertrophy induced by chronic intermittent hypoxia.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Metabolic regulation of ferroptosis in cancer: mechanisms, pharmacological inducers, and translational challenges.Apoptosis : an international journal on programmed cell death · 2026Review
- IRF9-dependent transcriptional regulation of SLC40A1 suppresses ferroptosis in dilated cardiomyopathy.Scientific reports · 2026Article
- Mechanisms driving resistance to oxidative stress during endometrial stromal cell decidualization†.Biology of reproduction · 2026Review
- Iron Metabolism in Cardiovascular Disease.Advances in experimental medicine and biology · 2025Review
- Cardiomyocyte-specific overexpression of FPN1 diminishes cardiac hypertrophy induced by chronic intermittent hypoxia.Journal of cellular and molecular medicine · 2024Article
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Authors and funding
12 authors.
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Abstract
The significance of iron in myocardial mitochondria function cannot be underestimated, because deviations in iron levels within cardiomyocytes may have profound detrimental effects on cardiac function. In this study, we investigated the effects of ferroportin 1 (FPN1) on cardiac iron levels and pathological alterations in mice subjected to chronic intermittent hypoxia (CIH). The cTNT-FPN1 plasmid was administered via tail vein injection to induce the mouse with FPN1 overexpression in the cardiomyocytes. CIH was established by exposing the mice to cycles of 21%-5% FiO
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