ArticleSTAR protocols2021
Optimization of mito-roGFP protocol to measure mitochondrial oxidative status in human coronary artery endothelial cells.
Article in STAR protocols, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- TR-107, a novel mitochondrial ClpP agonist, induces robust antitumor activity against preclinical models of adrenocortical carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Article
- Mitochondrial translation is the primary determinant of secondary mitochondrial complex I deficiencies.iScience · 2024Article
- NDUFS4 regulates cristae remodeling in diabetic kidney disease.Nature communications · 2024Article
- Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2024Article
- COX17 acetylation via MOF-KANSL complex promotes mitochondrial integrity and function.Nature metabolism · 2023Article
- Genetically Encoded Biosensors for the Fluorescence Detection of OSensors (Basel, Switzerland) · 2023Review
- Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction.Basic research in cardiology · 2023Article
- Methods to Study Mitochondria: Techniques Used to Study the Effects of Age-Related Diseases Including Alzheimer's.Current protocols · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) are implicated in endothelial dysfunction and cardiovascular disease. Endothelial cells (ECs) produce most ATP through glycolysis rather than oxidative phosphorylation; thus mitochondrial ROS production is lower than in other cell types. This makes quantification of changes in EC mitochondrial oxidative status challenging. Here, we present an optimized protocol using mitochondrial-targeted adenovirus-based redox sensor for ratiometric quantification of specific changes in mitochondrial ROS in live human coronary artery EC. For complete details on the use and execution of this protocol, please refer to Waypa et al
Indexed as
Identifiers
What OpenQuestion holds
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.