ArticlePloS one2020
Bach1 promotes muscle regeneration through repressing Smad-mediated inhibition of myoblast differentiation.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- BACH1 orchestrates macrophage state transitions to coordinate regenerative inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Functional role of THRAP3 in modulating thyroid hormone-mediated gene networks in C2C12 myotubes.PloS one · 2026Article
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Integrative ATAC-seq and RNA-seq Analysis of the Longissimus Dorsi Muscle of Gannan Yak and Jeryak.International journal of molecular sciences · 2024Article
- Bleomycin-treated myoblasts undergo p21-associated cellular senescence and have severely impaired differentiation.GeroScience · 2024Article
- Knockdown of Bach1 protects periodontal bone regeneration from inflammatory damage.Journal of cellular and molecular medicine · 2023Article
- The KEAP1-NRF2 pathway regulates TFEB/TFE3-dependent lysosomal biogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- BACH1 regulates the proliferation and odontoblastic differentiation of human dental pulp stem cells.BMC oral health · 2022Article
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Cancer-Related Cachexia: The Vicious Circle between Inflammatory Cytokines, Skeletal Muscle, Lipid Metabolism and the Possible Role of Physical Training.International journal of molecular sciences · 2022Review
- Contribution of the Transcription Factors Sp1/Sp3 and AP-1 toInternational journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported that Bach1-deficient mice show reduced tissue injuries in diverse disease models due to increased expression of heme oxygenase-1 (HO-1)that possesses an antioxidant function. In contrast, we found that Bach1 deficiency in mice exacerbated skeletal muscle injury induced by cardiotoxin. Inhibition of Bach1 expression in C2C12 myoblast cells using RNA interference resulted in reduced proliferation, myotube formation, and myogenin expression compared with control cells. While the expression of HO-1 was increased by Bach1 silencing in C2C12 cells, the reduced myotube formation was not rescued by HO-1 inhibition. Up-regulations of Smad2, Smad3 and FoxO1, known inhibitors of muscle cell differentiation, were observed in Bach1-deficient mice and Bach1-silenced C2C12 cells. Therefore, Bach1 may promote regeneration of muscle by increasing proliferation and differentiation of myoblasts.
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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.