ArticleDiabetologia2016
BNIP3 is essential for mitochondrial bioenergetics during adipocyte remodelling in mice.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Association of HIF1α, BNIP3, and BNIP3L with Hypoxia-Related Metabolic Stress in Metabolic Syndrome.Medicina (Kaunas, Lithuania) · 2026Article
- Targeted regulation of adipose tissue macrophages from an immunometabolic perspective: a novel therapeutic approach for obesity-related metabolic disorders.Frontiers in immunology · 2026Review
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Mitophagy is required to protect against excessive skeletal muscle atrophy following hindlimb immobilization.Journal of biomedical science · 2025Article
- Mitophagy Responds to the Environmental Temperature and Regulates Mitochondrial Mass in Adipose Tissues.Advances in experimental medicine and biology · 2024Review
- The autophagic regulation of rosiglitazone-promoted adipocyte browning.Frontiers in pharmacology · 2024Article
- The role of low-carbohydrate, high-fat diet in modulating autophagy and endoplasmic reticulum stress in aortic endothelial dysfunction of metabolic syndrome animal model.Frontiers in nutrition · 2024Article
- Crosstalk between mitochondrial biogenesis and mitophagy to maintain mitochondrial homeostasis.Journal of biomedical science · 2023Review
- Article
- Mitochondrial regulation and white adipose tissue homeostasis.Trends in cell biology · 2022Review
- IGFBP-3 functions as a molecular switch that mediates mitochondrial and metabolic homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Cistanche promotes the adipogenesis of 3T3-L1 preadipocytes.PloS one · 2022Article
- Oroxylin A ameliorates AKI-to-CKD transition through maintaining PPARα-BNIP3 signaling-mediated mitochondrial homeostasis.Frontiers in pharmacology · 2022Article
- Mitochondrial metabolism is a key regulator of the fibro-inflammatory and adipogenic stromal subpopulations in white adipose tissue.Cell stem cell · 2021Article
- STK3/STK4 signalling in adipocytes regulates mitophagy and energy expenditure.Nature metabolism · 2021Article
- Predictive network modeling in human induced pluripotent stem cells identifies key driver genes for insulin responsiveness.PLoS computational biology · 2020Article
- Significance of Soluble CD93 in Type 2 Diabetes as a Biomarker for Diabetic Nephropathy: Integrated Results from Human and Rodent Studies.Journal of clinical medicine · 2020Article
- The role of autophagy in brown and beige adipose tissue plasticity.Journal of physiology and biochemistry · 2020Review
- The Role of Autophagy in White Adipose Tissue Function: Implications for Metabolic Health.Metabolites · 2020Review
- Bnip3 regulates airway smooth muscle cell focal adhesion and proliferation.American journal of physiology. Lung cellular and molecular physiology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisAdipose tissue is a highly versatile system in which mitochondria in adipocytes undergo significant changes during active tissue remodelling. BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) is a mitochondrial protein and a known mitochondrial quality regulator. In this study, we investigated the role of BNIP3 in adipocytes, specifically under conditions of peroxisome proliferator-activated receptor-γ (PPARγ)-induced adipose tissue remodelling.
methodsThe expression of BNIP3 was evaluated in 3T3-L1 adipocytes in vitro, C57BL/6 mice fed a high-fat diet and db/db mice in vivo. Mitochondrial bioenergetics was investigated in BNIP3-knockdown adipocytes after rosiglitazone treatment. A putative peroxisome proliferator hormone responsive element (PPRE) was characterised by promoter assay and electrophoretic mobility shift assay (EMSA).
resultsThe protein BNIP3 was more abundant in brown adipose tissue than white adipose tissue. Furthermore, BNIP3 expression was upregulated by 3T3-L1 pre-adipocyte differentiation, starvation and rosiglitazone treatment. Conversely, BNIP3 expression in adipocytes decreased under various conditions associated with insulin resistance. This downregulation of BNIP3 was restored by rosiglitazone treatment. Knockdown of BNIP3 in adipocytes inhibited rosiglitazone-induced mitochondrial biogenesis and function, partially mediated by the 5' AMP-activated protein kinase (AMPK)-peroxisome proliferator-activated receptor γ, co-activator 1 α (PGC1α) signalling pathway. Rosiglitazone treatment increased the transcription level of Bnip3 in the reporter assay and the presence of the PPRE site in the Bnip3 promoter was demonstrated by EMSA. CONCLUSIONS/
interpretationThe protein BNIP3 contributes to the improvement of mitochondrial bioenergetics that occurs on exposure to rosiglitazone. It may be a novel therapeutic target for restoring mitochondrial dysfunction under insulin-resistant conditions.
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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.