ArticleScientific reports2017
Florfenicol-induced Mitochondrial Dysfunction Suppresses Cell Proliferation and Autophagy in Fibroblasts.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 42 citations in OpenAlex.
- Mitochondrial dynamics imbalance in hepatocellular carcinoma: from molecular mechanisms to new strategies for targeted therapy.Translational cancer research · 2026Review
- Syringin protects high glucose-induced BMSC injury, cell senescence, and osteoporosis by inhibiting JAK2/STAT3 signaling.Journal of applied biomedicine · 2024Article
- Development and in vitro evaluation of a lignin-PLGA nanocarrier for florfenicol delivery.Veterinary research communications · 2024Article
- Proteomic Analysis of the Mitochondrial Responses in P19 Embryonic Stem Cells Exposed to Florfenicol.Toxics · 2023Article
- Comparative Study on Synergistic Toxicity of Enrofloxacin Combined with Three Antibiotics on Proliferation of THLE-2 Cell.Antibiotics (Basel, Switzerland) · 2022Article
- Study on the mechanism of Salvia miltiorrhiza polysaccharides in relieving liver injury of broilers induced by florfenicol.Environmental science and pollution research international · 2022Article
- Molecular Mechanisms Underlying the Inhibition of Proliferation and Differentiation by Florfenicol in P19 Stem Cells: Transcriptome Analysis.Frontiers in pharmacology · 2022Article
- Effective therapeutic strategies in a preclinical mouse model of Charcot-Marie-Tooth disease.Human molecular genetics · 2021Article
- PFP@PLGA/CuNano convergence · 2021Article
- Enhanced Pharmaceutically Active Compounds Productivity fromMolecules (Basel, Switzerland) · 2021Article
- Florfenicol induces renal toxicity in chicks by promoting oxidative stress and apoptosis.Environmental science and pollution research international · 2021Article
- Low and high concentrations of butyrate regulate fat accumulation in chicken adipocytes via different mechanisms.Adipocyte · 2020Article
- Growth and cardiovascular development are repressed by florfenicol exposure in early chicken embryos.Poultry science · 2020Article
- Stereoisomer-specific ginsenoside 20(Journal of ginseng research · 2020Article
- Anti-inflammatory effects of Chinese propolis in lipopolysaccharide-stimulated human umbilical vein endothelial cells by suppressing autophagy and MAPK/NF-κB signaling pathway.Inflammopharmacology · 2019Article
- The Delicate Equilibrium between Oxidants and Antioxidants in Brain Glioma.Current neuropharmacology · 2019Review
- Teaching the basics of reactive oxygen species and their relevance to cancer biology: Mitochondrial reactive oxygen species detection, redox signaling, and targeted therapies.Redox biology · 2018Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Florfenicol (FLO) is one of the most popular antibiotics used in veterinary clinic and aquaculture. FLO can inhibit both bacterial and mitochondrial protein synthesis. However, the effects of FLO on mitochondrial function and cellular homeostasis remain unclear. Here we show that FLO inhibits expression of mitochondrial DNA-encoded proteins, decreases mitochondrial membrane potential, and promotes generation of reactive oxygen species (ROS) in vitro. As a result, activities of mitochondrial respiratory chain complex I and IV and the cellular ATP level are decreased and mitochondrial morphology is damaged. FLO represses cell growth and proliferation by suppression of phosphorylation of p70S6K through AMPK/mTOR/p70S6K pathway. Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway. Moreover, the clearance of damaged mitochondria by autophagy is impaired, leading to cell proliferation inhibition and promotes cell senescence. In addition, FLO-induced upregulation of cytosolic p53 may contribute to mitophagy deficiency via regulation of Parkin recruitment. In summary, our data suggest that florfenicol is an inhibitor of mitochondrial protein synthesis that can induce noticeable cytotoxicity. Thus, these findings can be useful for guiding the proper use of FLO and the development of safe drugs.
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.