ArticleScientific reports2023
Evaluation of drug-induced liver toxicity of trovafloxacin and levofloxacin in a human microphysiological liver model.
Article in Scientific reports, 2023. 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, 20 citations in OpenAlex.
- Therapeutic Ultrasound Versus Levofloxacin in Lipopolysaccharide-Induced Orchitis: Comparative Effects on Testicular Inflammation and Tissue Recovery in Rats.Iranian journal of pathology · 2026Article
- Strengthening Signal Detection in Pharmacovigilance by Using International Nonproprietary Name (INN) Stems.Drug safety · 2026Review
- Pannexins in the heart: cell-specific expression and contributions to disease.Cell and tissue research · 2026Review
- Panx1 and drug discovery: from non-specific inhibitors to tailored drug compounds.Cell and tissue research · 2026Review
- Secondary bile acid lithocholic acid ameliorates colitis-like inflammation in a human intestine-on-chip system.Frontiers in immunology · 2026Article
- Succinic acid enhances sedative activity of diazepam through GABAergic receptor modulation: Evidence from behavioral approach and computational insights.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Fluoroquinolones directly drive mitochondrial hyperpolarization and modulate iNOS expression in monocyte-derived macrophage populations.Discovery immunology · 2025Article
- Digital twin-enhanced three-organ microphysiological system for studying drug pharmacokinetics in pregnant women.Frontiers in pharmacology · 2025Article
- High-Scale 3D-Bioprinting Platform for the Automated Production of Vascularized Organs-on-a-Chip.Advanced healthcare materials · 2024Article
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-induced liver injury induced by already approved substances is a major threat to human patients, potentially resulting in drug withdrawal and substantial loss of financial resources in the pharmaceutical industry. Trovafloxacin, a broad-spectrum fluoroquinolone, was found to have unexpected side effects of severe hepatotoxicity, which was not detected by preclinical testing. To address the limitations of current drug testing strategies mainly involving 2D cell cultures and animal testing, a three-dimensional microphysiological model of the human liver containing expandable human liver sinusoidal endothelial cells, monocyte-derived macrophages and differentiated HepaRG cells was utilized to investigate the toxicity of trovafloxacin and compared it to the structurally-related non-toxic drug levofloxacin. In the model, trovafloxacin elicited vascular and hepatocellular toxicity associated with pro-inflammatory cytokine release already at clinically relevant concentrations, whereas levofloxacin did not provoke tissue injury. Similar to in vivo, cytokine secretion was dependent on a multicellular immune response, highlighting the potential of the complex microphysiological liver model for reliably detecting drug-related cytotoxicity in preclinical testing. Moreover, hepatic glutathione depletion and mitochondrial ROS formation were elucidated as intrinsic toxicity mechanisms contributing to trovafloxacin toxicity.
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.