ArticleStem cell research & therapy2023
COX6A2 deficiency leads to cardiac remodeling in human pluripotent stem cell-derived cardiomyocytes.
Article in Stem cell research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Mechanism of FoxO1 in the Metabolic Shift of Fetal Rat Heart.Molecules (Basel, Switzerland) · 2026Article
- Ethambutol induces optic neuropathy through SDHB-mediated ferroptosis in retinal ganglion cells via Smad4 pathway.Human cell · 2026Article
- Optimization of gene knockout approaches and sgRNA selection in hPSCs with inducible Cas9 expression.Scientific reports · 2025Article
- Metabolism-related gene PDK1 regulates myocardial cell remodeling and its mechanism.Stem cell research & therapy · 2025Article
- Comparative transcriptomics of iPSC-derived cardiomyocytes in a high and a low altitude population.bioRxiv : the preprint server for biology · 2025Article
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- Connexin 43 suppression enhances contractile force in human iPSC-derived cardiac tissues.Frontiers in bioengineering and biotechnology · 2025Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundCardiac remodeling is the initiating factor for the development of heart failure, which can result from various cardiomyopathies. Cytochrome c oxidase subunit 6A2 (COX6A2) is one of the components of cytochrome c oxidase that drives oxidative phosphorylation. The pathogenesis of myocardial remodeling caused by COX6A2 deficiency in humans remains unclear because there are no suitable research models. In this study, we established a COX6A2-deficient human cardiac myocyte (CM) model that mimics the human COX6A2 homozygous mutation and determined the effects of COX6A2 dysfunction and its underlying mechanism.
methodsA human COX6A2 homozygous knockout cardiomyocyte model was established by combining CRISPR/Cas9 gene editing technology and hiPSC-directed differentiation technology. Cell model phenotypic assays were done to characterize the pathological features of the resulting COX6A2-deficient cardiomyocytes.
resultsCOX6A2 gene knockout did not affect the pluripotency and differentiation efficiency of hiPSCs. Myocardial cells with a COX6A2 gene knockout showed abnormal energy metabolism, increased oxidative stress levels, abnormal calcium transport activity, and decreased contractility. In addition, L-carnitine and trimetazidine significantly improved energy metabolism in the COX6A2-deficient human myocardial model.
conclusionsWe have established a COX6A2-deficient human cardiomyocyte model that exhibits abnormal energy metabolism, elevated oxidative stress levels, abnormal calcium transport, and reduced contractility. This model represents an important tool to gain insight into the mechanism of action of energy metabolism disorders resulting in myocardial remodeling, elucidate the gene-phenotype relationship of COX6A2 deficiency, and facilitate drug screening.
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