ArticleCell death discovery2022
Disturbance of calcium homeostasis and myogenesis caused by TET2 deletion in muscle stem cells.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Pathological calcium overload impairs skeletal muscle regeneration through sustained NFAT-dependent proliferative signaling.Experimental & molecular medicine · 2026Article
- Exercise-related microRNAs in Caenorhabditis elegans regulate calcium homeostasis and mitochondrial dynamics: Conserved pathways, divergent microRNAs.The FEBS journal · 2026Article
- Semaglutide targets muscle mitochondria to regulate glutamine metabolism and treat osteoarthritis.iScience · 2026Article
- Mechanical Signaling Regulates DNA Methylation to Maintain Muscle Stem Cell Quiescence.bioRxiv : the preprint server for biology · 2026Article
- Transcriptional and epigenetic regulation of CaBioinformatics advances · 2026Article
- TET exhibits enzymatic-independent and-dependent functions during Drosophila flight muscle development and aging.Skeletal muscle · 2025Article
- Optimizing fatty acids composition in meat-like tissue derived from myogenic conversion of pig fibroblasts.Communications biology · 2025Article
- Article
- SYISL Knockout Promotes Embryonic Muscle Development of Offspring by Modulating Maternal Gut Microbiota and Fetal Myogenic Cell Dynamics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- Article
- Retinoic acid signalling inhibits myogenesis by blocking MYOD translation in pig skeletal muscle cells.Animal biotechnology · 2024Article
- Skeletal muscle TET3 promotes insulin resistance through destabilisation of PGC-1α.Diabetologia · 2024Article
- An Updated Review on the Significance of DNA and Protein Methyltransferases and De-methylases in Human Diseases: From Molecular Mechanism to Novel Therapeutic Approaches.Current medicinal chemistry · 2024Review
- Transcriptome analysis reveals the regulatory mechanism of myofiber development in male and female black Muscovy duck at different ages.Frontiers in veterinary science · 2024Article
- Article
- Delayed denervation-induced muscle atrophy inFrontiers in physiology · 2023Article
- Nrf2Frontiers in genetics · 2023Article
- Muscle injury causes long-term changes in stem-cell DNA methylation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Comparative Transcriptomic Analysis of mRNAs, miRNAs and lncRNAs in theBiomolecules · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle myogenesis is a sophisticated process controlled by genetic and epigenetic regulators. In animals, one of the key enzymes for the DNA demethylation of 5-methylcytosine is TET2. Although TET2 is essential for muscle development, the mechanisms by which TET2 regulates myogenesis, particularly the implication for muscle stem cells, remains unclear. In the present study, we employed the TET2 knockout mouse model to investigate the function of TET2 in muscle development and regeneration. We observed that TET2 deficiency caused impaired muscle stem cell proliferation and differentiation, resulting in the reduction in both myofiber number and muscle tissue size. Specifically, TET2 maintains calcium homeostasis in muscle stem cells by controlling the DNA methylation levels of the calcium pathway genes. Forced expression of the sodium/calcium exchanger protein SLC8A3 could rescue the myogenic defects in TET2 knockout cells. Our data not only illustrated the vital function of TET2 during myogenesis but also identified novel targets that contribute to calcium homeostasis for enhancing muscle function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.