ArticleCell death & disease2022
BNIP3 (BCL2 interacting protein 3) regulates pluripotency by modulating mitochondrial homeostasis via mitophagy.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- MUC1 Protects Preimplantation Embryos In Vitro via Clearance of ROS by Triggering Mitophagy.Cells · 2026Article
- Mitochondrial Homeostasis in Diabetic Cardiomyopathy: From Dysfunction to Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Advances in natural compounds modulating autophagy for the therapeutic intervention of heart failure.Molecular and cellular biochemistry · 2026Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- BNIP3 induced by hypoxia supports the survival of mesenchymal stromal cells (MSCs) after intravenous cell transplantation.Regenerative therapy · 2025Article
- Molecular regulation of mitophagy signaling in tumor microenvironment and its targeting for cancer therapy.Cytokine & growth factor reviews · 2025Review
- Mechanisms Underlying Muscle-Related Diseases and Aging: Insights into Pathophysiology and Therapeutic Strategies.Muscles (Basel, Switzerland) · 2025Review
- Long-Term Hypoxia Upregulates Wnt and TGFβ1 Signaling in Eccrine Sweat Gland Cells In Vitro.International journal of molecular sciences · 2025Article
- Review
- Unraveling key transposable elements in pathogen-induced bovine mastitis through comparative in vivo and in vitro transcriptomic analysis.BMC genomics · 2025Article
- Autophagy and the peroxisome proliferator-activated receptor signaling pathway: A molecular ballet in lipid metabolism and homeostasis.Molecular and cellular biochemistry · 2025Review
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Replicative Senescence in Mesenchymal Stem Cells: An In Vitro Study on Mitochondrial Dynamics and Metabolic Alterations.Antioxidants (Basel, Switzerland) · 2025Article
- DNM1L-mediated fission governs mitophagy & mitochondrial biogenesis during myogenic differentiation.Cell communication and signaling : CCS · 2025Article
- PTBP2 promotes cell survival and autophagy in chronic myeloid leukemia by stabilizing BNIP3.Cell death & disease · 2025Article
- The role of mitochondrial biogenesis, mitochondrial dynamics and mitophagy in gastrointestinal tumors.Cancer cell international · 2025Review
- Dysregulation of Mitochondrial Homeostasis in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mitochondrial DNA depletion syndrome and its cardiac complication.Frontiers in cardiovascular medicine · 2025Review
- Calcium-mediated regulation of mitophagy: implications in neurodegenerative diseases.npj metabolic health and disease · 2025Review
- Mitophagy Regulates Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy-mediated mitochondrial degradation plays pivotal roles in both the acquisition and maintenance of pluripotency, but the molecular mechanisms that link autophagy-mediated mitochondrial homeostasis to pluripotency regulation are unclear. Here, we identified that the mitophagy receptor BNIP3 regulates pluripotency. In mouse ESCs, depletion of BNIP3 caused accumulation of aberrant mitochondria accompanied by decreased mitochondrial membrane potential, increased production of reactive oxygen species (ROS), and reduced ATP generation, which led to compromised self-renewal and differentiation. Impairment of mitophagy by knockdown of BNIP3 inhibited mitochondrial clearance during pluripotency induction, resulting in decreased reprogramming efficiency. These defects were rescued by reacquisition of wild-type but not LIR-deficient BNIP3 expression. Taken together, our findings highlight a critical role of BNIP3-mediated mitophagy in the induction and maintenance of pluripotency.
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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.