ArticlePloS one2017
BGP-15 Protects against Oxidative Stress- or Lipopolysaccharide-Induced Mitochondrial Destabilization and Reduces Mitochondrial Production of Reactive Oxygen Species.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
- BGP-15 ameliorates sepsis-induced cardiomyopathy via SIRT3/SOD2-associated antioxidant signaling and suppression of myocardial inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Mitochondrial quality control in human ageing and longevity.Nature metabolism · 2026Review
- Molecular mechanisms of ovarian fibrosis.Molecular human reproduction · 2026Review
- Organelle stress in NLRP3 inflammasome: a central mediator of neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- Biochemical Insights into the Effects of a Small Molecule Drug Candidate on Imatinib-Induced Cardiac Inflammation.International journal of molecular sciences · 2025Article
- Sperm oxidative damage acquired during seminal plasma removal for assisted reproductive technology is reduced by BGP-15.Journal of assisted reproduction and genetics · 2025Article
- Telomere length in offspring is determined by mitochondrial-nuclear communication at fertilization.Nature communications · 2025Article
- Mitophagy in relation to chronic inflammation/ROS in aging.Molecular and cellular biochemistry · 2025Review
- Review
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Promoting mitochondrial dynamics by inhibiting the PINK1-PRKN pathway to relieve diabetic nephropathy.Disease models & mechanisms · 2024Article
- Electroretinographical Analysis of the Effect of BGP-15 in Eyedrops for Compensating Global Ischemia-Reperfusion in the Eyes of Sprague Dawley Rats.Biomedicines · 2024Article
- Resolution of inflammation in chronic disease via restoration of the heat shock response (HSR).Cell stress & chaperones · 2024Review
- The Role of Lifestyle and Dietary Factors in the Development of Premature Ovarian Insufficiency.Antioxidants (Basel, Switzerland) · 2023Review
- Attenuation of PMParticle and fibre toxicology · 2023Article
- BGP-15 Protects against Doxorubicin-Induced Cell Toxicity via Enhanced Mitochondrial Function.International journal of molecular sciences · 2023Article
- Drug Candidate BGP-15 Prevents Isoproterenol-Induced Arrhythmias and Alters Heart Rate Variability (HRV) in Telemetry-Implanted Rats.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Mitochondria ROS and mitophagy in acute kidney injury.Autophagy · 2023Article
- Restoring Sperm Quality Post-Cryopreservation Using Mitochondrial-Targeted Compounds.Antioxidants (Basel, Switzerland) · 2022Article
- Female reproductive life span is extended by targeted removal of fibrotic collagen from the mouse ovary.Science advances · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) play a critical role in the progression of mitochondria-related diseases. A novel insulin sensitizer drug candidate, BGP-15, has been shown to have protective effects in several oxidative stress-related diseases in animal and human studies. In this study, we investigated whether the protective effects of BGP-15 are predominantly via preserving mitochondrial integrity and reducing mitochondrial ROS production. BGP-15 was found to accumulate in the mitochondria, protect against ROS-induced mitochondrial depolarization and attenuate ROS-induced mitochondrial ROS production in a cell culture model, and also reduced ROS production predominantly at the complex I-III system in isolated mitochondria. At physiologically relevant concentrations, BGP-15 protected against hydrogen peroxide-induced cell death by reducing both apoptosis and necrosis. Additionally, it attenuated bacterial lipopolysaccharide (LPS)-induced collapse of mitochondrial membrane potential and ROS production in LPS-sensitive U-251 glioma cells, suggesting that BGP-15 may have a protective role in inflammatory diseases. However, BGP-15 did not have any antioxidant effects as shown by in vitro chemical and cell culture systems. These data suggest that BGP-15 could be a novel mitochondrial drug candidate for the prevention of ROS-related and inflammatory disease progression.
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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.