ArticleThe Journal of clinical investigation2018
Zinc transporter Slc39a8 is essential for cardiac ventricular compaction.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 55 citations in OpenAlex.
- Unveiling the prognostic and therapeutic landscape of the zinc transporter protein SLC39A family in colorectal cancer through multi-omics and machine learning approaches.Clinical and experimental medicine · 2026Article
- Mechanisms and the Role of p38 MAPK Signaling in Doxorubicin-Induced Cardiotoxicity: A Review.International journal of general medicine · 2026Review
- Effect of Cumulative Zinc Doses on Papillary Muscle Contractions and the Zinc Finger Protein ZEB1.Biological trace element research · 2025Article
- SLC39A8-mediated zinc dyshomeostasis potentiates kidney disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Human genetic variants in SLC39A8 impact uptake and steady-state metal levels within the cell.Life science alliance · 2025Article
- Large-scale brainstem neuroimaging and genetic analyses provide new insights into the neuronal mechanisms of hypertension.HGG advances · 2025Article
- Transient Notch Activation Converts Pluripotent Stem Cell-Derived Cardiomyocytes Towards a Purkinje Fiber Fate.bioRxiv : the preprint server for biology · 2024Article
- Cellular zinc metabolism and zinc signaling: from biological functions to diseases and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Unlocking the brain's zinc code: implications for cognitive function and disease.Frontiers in biophysics · 2024Article
- Metallothionein 3 Potentiates Pulmonary Artery Smooth Muscle Cell Proliferation by Promoting Zinc-MTF1-ATG5 Axis-mediated Autophagosome Formation.International journal of biological sciences · 2024Article
- Impact of diffused versus vasculature targeted DNA damage on the heart of mice depleted of telomeric factor Ft1.Aging cell · 2023Article
- The role of Zn2+ in shaping intracellular Ca2+ dynamics in the heart.The Journal of general physiology · 2023Review
- Zinc in Cardiovascular Functions and Diseases: Epidemiology and Molecular Mechanisms for Therapeutic Development.International journal of molecular sciences · 2023Review
- Cardiovascular Diseases and Zinc.Biological trace element research · 2023Review
- Endothelial Loss of ETS1 Impairs Coronary Vascular Development and Leads to Ventricular Non-Compaction.Circulation research · 2022Article
- In ovo exposure to cadmium causes right ventricle hyperplasia due to cell proliferation of cardiomyocytes.Toxicology letters · 2022Article
- Interplay between ZnInternational journal of molecular sciences · 2022Review
- Coordination of iron homeostasis by bone morphogenetic proteins: Current understanding and unanswered questions.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Endocardial-Myocardial Interactions During Early Cardiac Differentiation and Trabeculation.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Isolated left ventricular noncompaction (LVNC) results from excessive trabeculation and impaired myocardial compaction during heart development. The extracellular matrix (ECM) that separates endocardium from myocardium plays a critical but poorly understood role in ventricular trabeculation and compaction. In an attempt to characterize solute carrier family 39 member 8-null (Slc39a8-null) mice, we discovered that homozygous null embryos do not survive embryogenesis and exhibit a cardiac phenotype similar to human LVNC. Slc39a8 encodes a divalent metal cation importer that has been implicated in ECM degradation through the zinc/metal regulatory transcription factor 1 (Zn/MTF1) axis, which promotes the expression of ECM-degrading enzymes, including Adamts metalloproteinases. Here, we have shown that Slc39a8 is expressed by endothelial cells in the developing mouse heart, where it serves to maintain cellular Zn levels. Furthermore, Slc39a8-null hearts exhibited marked ECM accumulation and reduction of several Adamts metalloproteinases. Consistent with the in vivo observations, knockdown of SLC39A8 in HUVECs decreased ADAMTS1 transcription by decreasing cellular Zn uptake and, as a result, MTF1 transcriptional activity. Our study thus identifies a gene underlying ventricular trabeculation and compaction development, and a pathway regulating ECM during myocardial morphogenesis.
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Registered trials
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