ArticleFrontiers in cell and developmental biology2020
Bach1 Inhibition Suppresses Osteoclastogenesis via Reduction of the Signaling via Reactive Oxygen Species by Reinforced Antioxidation.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanistic and Therapeutic Insights into Nrf2-Mediated Redox Regulation in Periodontitis.Antioxidants (Basel, Switzerland) · 2026Review
- Nrf2 as a redox checkpoint in autoimmune joint inflammation: microenvironmental redox control across the arthritis spectrum.Frontiers in immunology · 2026Review
- miR-629-3p affects postmenopausal osteoporosis through targeted regulation of BACH1.Journal of orthopaedic surgery and research · 2025Article
- Salvianolic Acid A Mitigates Osteoporotic Bone Loss by Repressing Reactive Oxygen Species via the Nrf2-HO-1 Pathway.Phytotherapy research : PTR · 2025Article
- A BACH1 inhibitor ameliorates myocardial infarction and limb ischemia in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Effect of natural compounds on NRF2/KEAP1 signaling in periodontitis: a potential use to prevent age-related disorders.Molecular biology reports · 2025Review
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- BACH1 as a key driver in rheumatoid arthritis fibroblast-like synoviocytes identified through gene network analysis.Life science alliance · 2025Article
- Loss of BACH1 improves osteogenic differentiation in glucocorticoid-induced hBMSCs through restoring autophagy.BMC musculoskeletal disorders · 2024Article
- Activation of Nuclear Factor Erythroid 2-Related Factor 2 Transcriptionally Upregulates Ectonucleotide Pyrophosphatase/Phosphodiesterase 1 Expression and Inhibits Ectopic Calcification in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Sinensetin protects against periodontitis through binding to Bach1 enhancing its ubiquitination degradation and improving oxidative stress.International journal of oral science · 2024Article
- Gene Network Analyses Identify Co-regulated Transcription Factors and BACH1 as a Key Driver in Rheumatoid Arthritis Fibroblast-like Synoviocytes.bioRxiv : the preprint server for biology · 2024Article
- Knockdown of Bach1 protects periodontal bone regeneration from inflammatory damage.Journal of cellular and molecular medicine · 2023Article
- Orientin suppresses osteoclastogenesis and ameliorates ovariectomy-induced osteoporosis via suppressing ROS production.Food science & nutrition · 2023Article
- Genetic dissection of triplicated chromosome 21 orthologs yields varying skeletal traits in Down syndrome model mice.Disease models & mechanisms · 2023Article
- Pathophysiological role of BACH transcription factors in digestive system diseases.Frontiers in physiology · 2023Review
- Harnessing the Therapeutic Potential of the Nrf2/Bach1 Signaling Pathway in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2022Review
- The Role of NRF2 in Bone Metabolism - Friend or Foe?Frontiers in endocrinology · 2022Review
- Nrf2 activator PB125® as a carnosic acid-based therapeutic agent against respiratory viral diseases, including COVID-19.Free radical biology & medicine · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone destructive diseases such as periodontitis are common worldwide and are caused by excessive osteoclast formation and activation. Receptor activator of nuclear factor-κB ligand (RANKL) is essential factor for osteoclastogenesis. This triggers reactive oxygen species (ROS), which has a key role in intracellular signaling as well exerting cytotoxicity. Cells have protective mechanisms against ROS, such as nuclear factor E2-related factor 2 (Nrf2), which controls the expression of many antioxidant enzyme genes. Conversely, BTB and CNC homology 1 (Bach1), a competitor for Nrf2, transcriptionally represses the expression of anti-oxidant enzymes. Previously, we demonstrated that RANKL induces Bach1 nuclear import and attenuates the expression of Nrf2-mediated antioxidant enzymes, thereby augmenting intracellular ROS signaling and osteoclastogenesis. However, it remains unknown if Bach1 inhibitors attenuate osteoclastogenesis. In this study, we hypothesized that Bach1 inhibition would exert an anti-osteoclastogenic effects via diminishing of intracellular ROS signaling through augmented antioxidation. We used RAW 264.7 cells as osteoclast progenitor cells. Using flow cytometry, we found that Bach1 inhibitors attenuated RANKL-mediated ROS generation, which resulted in the inhibition of osteoclastogenesis. Local injection of a Bach1 inhibitor into the calvaria of male BALB/c mice blocked bone destruction induced by lipopolysaccharide. In conclusion, we demonstrate that Bach1 inhibitor attenuates RANKL-mediated osteoclastogenesis and bone destruction in mice by inducing the expression of Nrf2-regulated antioxidant enzymes that consequently decrease intracellular ROS levels. Bach1 inhibitors have potential in inhibiting bone destructive diseases such as periodontitis, rheumatoid arthritis and osteoporosis.
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