ArticleAntimicrobial agents and chemotherapy2014
Colistin-induced nephrotoxicity in mice involves the mitochondrial, death receptor, and endoplasmic reticulum pathways.
Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 179 citations in OpenAlex.
- A bibliometric analysis of polymyxin-induced nephrotoxicity research: Trends and insights (2005-2024).Medicine · 2026Article
- Polymyxin antibiotics induce nephrotoxicity through the selective inhibition of Complex I-dependent respiration in mouse and rat mitochondria.Archives of toxicology · 2026Article
- Antimicrobial-induced hyponatremia: pathophysiological mechanisms, implicated agents, and clinical management strategies.European journal of clinical pharmacology · 2026Review
- Perspectives on Colistin-An Old Antibiotic with Renewed Relevance in Modern Medicine.International journal of molecular sciences · 2026Review
- An antimicrobial peptide as a potential therapy for bacterial pneumonia that alleviates antimicrobial resistance.Nature communications · 2025Article
- Molecular mechanisms attributed to colistin renal proximal tubular epithelial cytotoxicity.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Review
- Bakuchiol, a Natural Antioxidant, Synergizes with Colistin Against Multidrug-Resistant Gram-Negative Bacteria by Disrupting Iron Homeostasis and Membrane Integrity.Antioxidants (Basel, Switzerland) · 2025Article
- Antimicrobial Efficacy of Impregnated Human Acellular Dermal Substitutes in Burn Wound Models.Antibiotics (Basel, Switzerland) · 2025Article
- Corynoxeine Supplementation Ameliorates Colistin-Induced Kidney Oxidative Stress and Inflammation in Mice.Antioxidants (Basel, Switzerland) · 2025Article
- The α-Helical Amphipathic Peptide Alleviates Colistin-Induced Nephrotoxicity by Maintaining Mitochondrial Function in Both In Vitro and In Vivo Infection Models.Antibiotics (Basel, Switzerland) · 2025Article
- Direct exposure with exogenous mitochondria reduce colistin-induced mitochondrial dysfunction and cellular damages in isolated rat renal proximal tubular cells.Journal of molecular histology · 2025Article
- Metabolomics- and proteomics-based multi-omics integration reveals early metabolite alterations in sepsis-associated acute kidney injury.BMC medicine · 2025Article
- Examining the role of trans-sodium crocetinate in alleviating colistin-induced cytotoxicity through apoptosis and autophagy pathways on HEK-293 cells.Iranian journal of basic medical sciences · 2025Article
- Article
- Ellagic Acid Reduces Cadmium Exposure-Induced Apoptosis in HT22 Cells via Inhibiting Oxidative Stress and Mitochondrial Dysfunction and Activating Nrf2/HO-1 Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Evaluating nephrotoxicity reduction in a novel polymyxin B formulation: insights from a 3D kidney-on-a-chip model.Antimicrobial agents and chemotherapy · 2024Article
- L-carnitine co-administration prevents colistin-induced mitochondrial permeability transition and reduces the risk of acute kidney injury in mice.Scientific reports · 2024Article
- Mechanisms of gelofusine protection in an in vitro model of polymyxin B-associated renal injury.American journal of physiology. Renal physiology · 2024Article
- Antimicrobial Peptides towards Clinical Application-A Long History to Be Concluded.International journal of molecular sciences · 2024Review
- Dextrin conjugation to colistin inhibits its toxicity, cellular uptake and acute kidney injuryRSC pharmaceutics · 2024Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nephrotoxicity is the dose-limiting factor for colistin, but the exact mechanism is unknown. This study aimed to investigate the roles of the mitochondrial, death receptor, and endoplasmic reticulum pathways in colistin-induced nephrotoxicity. Mice were intravenously administered 7.5 or 15 mg of colistin/kg of body weight/day (via a 3-min infusion and divided into two doses) for 7 days. Renal function, oxidative stress, and apoptosis were measured. Representative biomarkers involved in the mitochondrial, death receptor, and endoplasmic reticulum pathways were investigated, and the key markers involved in apoptosis and autophagy were examined. After 7-day colistin treatment, significant increase was observed with blood urea nitrogen, serum creatinine, and malondialdehyde, while activities of superoxide dismutase (SOD) and catalase decreased in the kidneys. Acute tubular necrosis and mitochondrial dysfunction were detected, and colistin-induced apoptosis was characterized by DNA fragmentation, cleavage of poly(ADP-ribose) polymerase (PARP-1), increase of 8-hydroxydeoxyguanosine (8-OHdG), and activation of caspases (caspase-8, -9, and -3). It was evident that colistin-induced apoptosis involved the mitochondrial pathway (downregulation of Bcl-2 and upregulation of cytochrome C [cytC] and Bax), death receptor pathway (upregulation of Fas, FasL, and Fas-associated death domain [FADD]), and endoplasmic reticulum pathway (upregulation of Grp78/Bip, ATF6, GADD153/CHOP, and caspase-12). In the 15-mg/kg/day colistin group, expression of the cyclin-dependent kinase 2 (CDK2) and phosphorylated JNK (p-JNK) significantly increased (P < 0.05), while in the 7.5-mg/kg/day colistin group, a large number of autophagolysosomes and classic autophagy were observed. Western blot results of Beclin-1 and LC3B indicated that autophagy may play a protective role in colistin-induced nephrotoxicity. In conclusion, this is the first study to demonstrate that all three major apoptosis pathways and autophagy are involved in colistin-induced nephrotoxicity.
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