ArticleThe Journal of clinical investigation2021
BACH2 inhibition reverses β cell failure in type 2 diabetes models.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 68 citations in OpenAlex.
- Article
- Developmental and MAPK-responsive transcription factors regulate distinct malignant cell states and associated genetic dependencies in pancreatic cancer.Nature genetics · 2026Article
- pyVIPER: a fast and scalable Python package for protein activity estimation and master regulator analysis of single-cell RNA sequencing data.BMC bioinformatics · 2026Article
- Workload-induced changes to cell state contribute to β-cell failure in diabetes.bioRxiv : the preprint server for biology · 2026Article
- Article
- Multi-omics analysis identifies SMPD1 as a key contributor in sphingolipid pathway for Type 2 diabetes pathogenesis.Genes & genomics · 2026Article
- BACH transcription factors in diseases of the exocrine and endocrine pancreas: effects, mechanisms, and clinical implications.Frontiers in medicine · 2026Review
- Human pancreatic α-cell heterogeneity and trajectory inference analyses reveal SMOC1 as a β-cell dedifferentiation gene.Nature communications · 2025Article
- Insulin resistance in type 2 diabetes mellitus.Nature reviews. Endocrinology · 2025Review
- METTL3 mediates CPB1 expression by regulating transcription factor BACH2 to promote apoptosis and oxidative stress of lens epithelial cells.Journal of bioenergetics and biomembranes · 2025Article
- Identification and targeting of regulators of SARS-CoV-2-host interactions in the airway epithelium.Science advances · 2025Article
- Sensitivity analysis on protein-protein interaction networks through deep graph networks.BMC bioinformatics · 2025Article
- β-Cell Dedifferentiation in HOMA-βlow and HOMA-βhigh Subjects.The Journal of clinical endocrinology and metabolism · 2025Article
- Retrograde mitochondrial signaling governs the identity and maturity of metabolic tissues.Science (New York, N.Y.) · 2025Article
- The regulatory architecture of the primed pluripotent cell state.Nature communications · 2025Article
- A mechanism-informed deep neural network enables prioritization of regulators that drive cell state transitions.Nature communications · 2025Article
- Single-Cell RNA-seq Analysis Reveals a Positive Correlation between Ferroptosis and Beta-Cell Dedifferentiation in Type 2 Diabetes.Biomedicines · 2024Article
- LIPUS regulates the progression of knee osteoarthritis in mice through primary cilia-mediated TRPV4 channels.Apoptosis : an international journal on programmed cell death · 2024Article
- Review
- Cyb5r3 activation rescues secondary failure to sulfonylurea but not β-cell dedifferentiation.PloS one · 2024Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Type 2 diabetes (T2D) is associated with defective insulin secretion and reduced β cell mass. Available treatments provide a temporary reprieve, but secondary failure rates are high, making insulin supplementation necessary. Reversibility of β cell failure is a key translational question. Here, we reverse engineered and interrogated pancreatic islet-specific regulatory networks to discover T2D-specific subpopulations characterized by metabolic inflexibility and endocrine progenitor/stem cell features. Single-cell gain- and loss-of-function and glucose-induced Ca2+ flux analyses of top candidate master regulatory (MR) proteins in islet cells validated transcription factor BACH2 and associated epigenetic effectors as key drivers of T2D cell states. BACH2 knockout in T2D islets reversed cellular features of the disease, restoring a nondiabetic phenotype. BACH2-immunoreactive islet cells increased approximately 4-fold in diabetic patients, confirming the algorithmic prediction of clinically relevant subpopulations. Treatment with a BACH inhibitor lowered glycemia and increased plasma insulin levels in diabetic mice, and restored insulin secretion in diabetic mice and human islets. The findings suggest that T2D-specific populations of failing β cells can be reversed and indicate pathways for pharmacological intervention, including via BACH2 inhibition.
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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 Socratic graph.