ArticleEBioMedicine2020
Bach1-induced suppression of angiogenesis is dependent on the BTB domain.
Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Elevated BACH1 Contributes to Mitochondrial Succinylome Remodeling and Trophoblast Bioenergetic Dysfunction in Preeclampsia.Antioxidants (Basel, Switzerland) · 2026Article
- BPC157 drives angiogenesis through FBXO22-dependent stabilization of BACH1.Cell communication and signaling : CCS · 2026Article
- miR-629-3p affects postmenopausal osteoporosis through targeted regulation of BACH1.Journal of orthopaedic surgery and research · 2025Article
- A BACH1 inhibitor ameliorates myocardial infarction and limb ischemia in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Angiogenesis within atherosclerotic plaques: Mechanical regulation, molecular mechanism and clinical diagnosis.Mechanobiology in medicine · 2025Review
- Disruption of BACH1 Protects AC16 Cardiomyocytes Against Hypoxia/Reoxygenation-Evoked Injury by Diminishing CDKN3 Transcription.Cardiovascular toxicology · 2024Article
- Loss of BACH1 improves osteogenic differentiation in glucocorticoid-induced hBMSCs through restoring autophagy.BMC musculoskeletal disorders · 2024Article
- Ferroptosis regulation by Cap'n'collar family transcription factors.The Journal of biological chemistry · 2024Review
- Hsa_circ_0004872 alleviates meningioma progression by sponging miR-190a-3p/PTEN signaling.BMC cancer · 2024Article
- Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy.Biomarker research · 2024Review
- Antioxidants stimulate BACH1-dependent tumor angiogenesis.The Journal of clinical investigation · 2023Article
- BACH1-induced ferroptosis drives lymphatic metastasis by repressing the biosynthesis of monounsaturated fatty acids.Cell death & disease · 2023Article
- Mitophagy in atherosclerosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- Pathophysiological role of BACH transcription factors in digestive system diseases.Frontiers in physiology · 2023Review
- Article
- Signal amplification in the KEAP1-NRF2-ARE antioxidant response pathway.Redox biology · 2022Review
- HDAC1: an environmental sensor regulating endothelial function.Cardiovascular research · 2022Review
- Iron in Cancer Progression: Does BACH1 Promote Metastasis by Altering Iron Homeostasis?Sub-cellular biochemistry · 2022Article
- Targeting angiogenesis in myocardial infarction: Novel therapeutics (Review).Experimental and therapeutic medicine · 2022Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor Bach1 impairs angiogenesis after ischemic injury by suppressing Wnt/β-catenin signaling; however, the specific domains responsible for the anti-angiogenic effects of Bach1 remain unclear. This study determined the role of the BTB domain of Bach1 in ischemic angiogenesis. Bach1 is highly expressed in circulating endothelial cells from acute myocardial infarction patients and is the early induction gene after ischemia. Mice were treated with adenoviruses coding for GFP (AdGFP), Bach1 (AdBach1), or a Bach1 mutant lacking the BTB domain (AdBach1-ΔBTB) after surgically induced hind-limb ischemia. Measures of blood-flow recovery, capillary density, and the expression of vascular endothelial growth factor (VEGF) and heme oxygenase-1 (HO-1) were significantly lower and ROS levels were higher in the AdBach1 group, but not in AdBach1-ΔBTB animals. Furthermore, transfection with AdBach1, but not AdBach1-ΔBTB, in human endothelial cells was associated with significant declines in 1) capillary density and hemoglobin content in the Matrigel-plug assay, 2) proliferation, migration, tube formation, and VEGF and HO-1 expression in endothelial cells. Bach1 binds directly with TCF4, and this interaction is mediated by residues 81-89 of the Bach1 BTB domain and the N-terminal domain of TCF4. Bach1, but not Bach1-ΔBTB, also co-precipitated with histone deacetylase 1 (HDAC1), while the full-length HDAC1 proteins, but not HDAC1 mutants lacking the protein-interaction domain, co-precipitated with Bach1. Collectively, these results demonstrate that the anti-angiogenic activity of Bach1 is crucially dependent on molecular interactions that are mediated by the protein's BTB domain, and this domain could be a drug target for angiogenic therapy.
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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.