ArticleInternational journal of molecular sciences2021
Selenoprotein DIO2 Is a Regulator of Mitochondrial Function, Morphology and UPRmt in Human Cardiomyocytes.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Disrupted thyroid hormone-mitochondrial coupling in diabetic cardiomyopathy: a candidate upstream amplifier of metabolic and redox maladaptation.Frontiers in endocrinology · 2026Review
- Sex-specific cardiac remodeling and metabolic reprogramming in IUGR F2 fetuses following glyphosate or glyphosate-based herbicide exposure.Frontiers in toxicology · 2026Article
- Nano-Selenium supplementation Improves Meat Quality, Protein Deposition, and Selenoprotein Gene Expression in Channel Catfish (Ictalurus Punctatus).Biological trace element research · 2026Article
- Metabolic Functions and Mechanisms of Selenium, Selenocysteine, and GPX4 Mediated Immune Regulation Through Autophagy in Solid Tumors.Food science & nutrition · 2025Review
- Transcriptome-based analysis reveals relationship between duck eggshell color and eggshell strength.BMC genomics · 2025Article
- Micronutrient deficiencies and new-onset atrial fibrillation in a community-based cohort: data from PREVEND.Clinical research in cardiology : official journal of the German Cardiac Society · 2025Observational
- Mechanisms of the Mitochondrial Unfolded Protein Response in Caenorhabditis elegans and Mammals and Its Roles in Striated Muscles.Aging and disease · 2024Review
- Higher Peripheral Thyroid Sensitivity Is Linked to a Lower Risk of Heart Failure After Acute Myocardial Infarction.The Journal of clinical endocrinology and metabolism · 2023Article
- Thyroid hormone modulates hyperoxic neonatal lung injury and mitochondrial function.JCI insight · 2023Article
- The Physiological Functions and Polymorphisms of Type II Deiodinase.Endocrinology and metabolism (Seoul, Korea) · 2023Review
- CaInternational journal of molecular sciences · 2023Article
- Relationship between selenium status, selenoproteins and COVID-19 and other inflammatory diseases: A critical review.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2023Review
- Cross-Talk between the Cytokine IL-37 and Thyroid Hormones in Modulating Chronic Inflammation Associated with Target Organ Damage in Age-Related Metabolic and Vascular Conditions.International journal of molecular sciences · 2022Review
- Micronutrient deficiencies in heart failure: Mitochondrial dysfunction as a common pathophysiological mechanism?Journal of internal medicine · 2022Review
- Antisense Therapy Attenuates Phospholamban p.(Arg14del) Cardiomyopathy in Mice and Reverses Protein Aggregation.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Members of the fetal-gene-program may act as regulatory components to impede deleterious events occurring with cardiac remodeling, and constitute potential novel therapeutic heart failure (HF) targets. Mitochondrial energy derangements occur both during early fetal development and in patients with HF. Here we aim to elucidate the role of DIO2, a member of the fetal-gene-program, in pluripotent stem cell (PSC)-derived human cardiomyocytes and on mitochondrial dynamics and energetics, specifically. RNA sequencing and pathway enrichment analysis was performed on mouse cardiac tissue at different time points during development, adult age, and ischemia-induced HF. To determine the function of DIO2 in cardiomyocytes, a stable human hPSC-line with a DIO2 knockdown was made using a short harpin sequence. Firstly, we showed the selenoprotein, type II deiodinase (DIO2): the enzyme responsible for the tissue-specific conversion of inactive (T4) into active thyroid hormone (T3), to be a member of the fetal-gene-program. Secondly, silencing DIO2 resulted in an increased reactive oxygen species, impaired activation of the mitochondrial unfolded protein response, severely impaired mitochondrial respiration and reduced cellular viability. Microscopical 3D reconstruction of the mitochondrial network displayed substantial mitochondrial fragmentation. Summarizing, we identified DIO2 to be a member of the fetal-gene-program and as a key regulator of mitochondrial performance in human cardiomyocytes. Our results suggest a key position of human DIO2 as a regulator of mitochondrial function in human cardiomyocytes.
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Registered trials
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