ArticleFrontiers in genetics2020
Quantitative Proteomic Profiling of Mitochondrial Toxicants in a Human Cardiomyocyte Cell Line.
Article in Frontiers in genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Expanded Tox21 Biological Assay Panel for the Prediction of Drug-Induced Liver Injury and Cardiotoxicity.Environmental health perspectives · 2026Article
- Triphenylphosphonium compounds preferentially inhibit long-chain fatty acid oxidation in cardiac mitochondria.Research square · 2026Article
- Toxicometabolomics-based cardiotoxicity evaluation of Thiazolidinedione exposure in human-derived cardiomyocytes.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- High-Throughput Screening to Advance In Vitro Toxicology: Accomplishments, Challenges, and Future Directions.Annual review of pharmacology and toxicology · 2024Review
- Molecular and functional profiling of cell diversity and identity in the lateral superior olive, an auditory brainstem center with ascending and descending projections.Frontiers in cellular neuroscience · 2024Article
- Mitochondrial Membrane Potential Assay.Methods in molecular biology (Clifton, N.J.) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Mitochondria are essential cellular organelles that participate in important cellular processes, including bioenergetics, metabolism, and signaling. Recent functional and proteomic studies have revealed the remarkable complexity of mitochondrial protein organization. Mitochondrial protein machineries with diverse functions such as protein translocation, respiration, metabolite transport, protein quality control and the control of membrane architecture interact with each other in dynamic networks. The goal of this study was to identify protein expression changes in a human cardiomyocyte cell line treated with several mitochondrial toxicants which inhibit mitochondrial membrane potential (MMP) and mitochondrial respiration. AC16 human cardiomyocyte cells were treated with carbonyl cyanide
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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.