Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (607 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Glycosylated compounds in which there is an amino substituent on the glycoside. Some of them are clinically important antibiotics.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Aminoglycoside.
Where it fits in the MeSH classification
- Broader topics
- Glycosides
- Narrower topics
- Anthracyclines; Butirosin Sulfate; Calicheamicins; Gentamicins; Hygromycin B; Kanamycin; Metrizamide; Neomycin; Paromomycin; Puromycin; Spectinomycin; Streptomycin; Streptothricins; Streptozocin
- See also
- Amino Sugars
Related concepts
- Antibiotics
Research landscape
PubMed indexes 181,388 records tagged with the MeSH heading “Aminoglycosides” (counts retrieved 2026-10-31). 25,257 of them (13.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 86,765 records.
Reviews account for 9,327 records (5.1%) and meta-analyses for 640. Randomized controlled trials number 7,055 (3.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 86,765 |
| 2000-2009 | 28,910 |
| 2010-2019 | 40,456 |
| 2020 onward | 25,257 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 9,327 | 5.1% |
| Meta-analyses | 640 | 0.4% |
| Randomized controlled trials | 7,055 | 3.9% |
Method: PubMed query "Aminoglycosides"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Targeting the powerhouse: the mitochondrial perspective on gentamicin-induced kidney injury | 2026 | Review article Design not recorded in structured metadata | 5 | cc by PMID 41654647 · DOI · PMC13086777 |
| A systematic literature review and (network) meta-analysis of the effectiveness of ceftolozane/tazobactam versus aminoglycosides/polymyxins and ceftazidime/avibactam for treating adult patients with multidrug-resistant Pseudomonas aeruginosa infections | 2026 | Systematic review Design not recorded in structured metadata | 5 | cc by PMID 41532768 · DOI · PMC12888884 |
| Synergy between immune system and antibiotics drives infection control in mice | 2025 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41646972 · DOI · PMC12868242 |
Targeting the powerhouse: the mitochondrial perspective on gentamicin-induced kidney injury [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Gentamicin (GEN), an aminoglycoside antibiotic, induces nephrotoxicity primarily via mitochondrial dysfunction.
- Closing excerpt
- Overall, preserving mitochondrial function represents a promising avenue for reducing nephrotoxicity while maintaining the antibacterial efficacy of GEN.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (176 words)
Gentamicin (GEN), an aminoglycoside antibiotic, induces nephrotoxicity primarily via mitochondrial dysfunction. This review summarizes mechanisms including reactive oxygen species (ROS) overproduction, mitochondrial DNA (mtDNA) damage, impairment of oxidative phosphorylation, and mitochondrial permeability transition pore (mPTP) activation. These mitochondrial alterations lead to adenosine triphosphate (ATP) depletion, apoptosis, and renal injury. In addition to apoptotic pathways, necrotic cell death can also be triggered, further aggravating kidney damage. Furthermore, GEN has been reported to directly interfere with mitochondrial ribosomes and gene expression, highlighting mitochondria as both targets and amplifiers of cellular toxicity. Therapeutic approaches targeting mitochondrial integrity, including antioxidants and mitochondrial transplantation, demonstrate potential nephroprotection. Additional strategies such as mPTP, stimulation of mitochondrial biogenesis, and pharmacological modulators of mitochondrial respiration have also shown promise in experimental studies. Understanding mitochondrial mechanisms underlying gentamicin-induced renal injury is crucial for developing targeted therapeutic strategies. A more comprehensive knowledge of mitochondrial regulation, organelle crosstalk, and early biomarkers of dysfunction will facilitate translation into clinical practice. Overall, preserving mitochondrial function represents a promising avenue for reducing nephrotoxicity while maintaining the antibacterial efficacy of GEN.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41654647 · DOI · PMC13086777
A systematic literature review and (network) meta-analysis of the effectiveness of ceftolozane/tazobactam versus aminoglycosides/polymyxins and ceftazidime/avibactam for treating adult patients with multidrug-resistant Pseudomonas aeruginosa infections [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Multidrug-resistantant (MDR) Pseudomonas aeruginosa is a major public health concern necessitating new antimicrobials.
- Closing excerpt
- Larger prospective studies with standardized outcome measures are needed to further inform clinical decision-making.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (253 words)
Multidrug-resistantant (MDR) Pseudomonas aeruginosa is a major public health concern necessitating new antimicrobials. There are new antimicrobials available with activity against MDR-P. aeruginosa, but there is a lack of robust evidence synthesis to guide clinical decision-making for patients with infections caused by MDR-P. aeruginosa. This study, which was supported by Merck & Co., Inc., aimed to evaluate the real-world effectiveness of ceftolozane/tazobactam (C/T) compared to other commonly used therapies (aminoglycosides/polymyxins and ceftazidime/avibactam [CZA]) among adults with MDR-P. aeruginosa infections. A systematic literature review was conducted to identify real-world clinical and healthcare-resource utilization outcomes for C/T versus comparators. A feasibility assessment excluded comparators that were not aminoglycosides/polymyxins or CZA due to insufficient data for comparisons. A meta-analysis and network meta-analysis (NMA) were conducted on the included studies. Heterogeneity between the studies was calculated using I2 statistic. The NMA displayed statistically significant results for clinical cure (odds ratio [OR] = 0.308, 95% CI = 0.168-0.515) and all-cause mortality (OR = 1.651, 95% CI = 1.114-2.501) for C/T versus aminoglycosides/polymyxins, while microbiological cure and length of stay did not display statistical significance. However, comparisons for C/T versus CZA demonstrated no statistical significance for any of the outcomes explored. These findings suggest that C/T is more likely to achieve clinical cure and less likely to result in all-cause mortality compared to aminoglycosides/polymyxins. In the absence of head-to-head trials, this real-world evidence indicates potential advantages of using C/T over aminoglycosides/polymyxins for MDR-P. aeruginosa infections. Larger prospective studies with standardized outcome measures are needed to further inform clinical decision-making.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41532768 · DOI · PMC12888884
Synergy between immune system and antibiotics drives infection control in mice [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundAntibiotics and host immunity are traditionally viewed as independent defenses, with antibiotics reducing bacterial load to levels manageable by the immune system.
- Closing excerpt
- They highlight the therapeutic potential of augmenting innate immune activation to improve infection outcomes, particularly in immunocompromised patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (178 words)
BackgroundAntibiotics and host immunity are traditionally viewed as independent defenses, with antibiotics reducing bacterial load to levels manageable by the immune system. Modeling studies, however, predict that synergy between these defenses is critical for infection control, but this has not been experimentally verified.MethodsWe tested this concept using a Pseudomonas aeruginosa wound infection model in immunocompetent (C57BL/6) and immunocompromised (NSG) mice treated with systemic tobramycin.ResultsIn C57BL/6 mice, tobramycin-mediated bacterial killing increased pathogen-associated molecular patterns (PAMPs) - namely lipopolysaccharide (LPS) - which in turn amplified local inflammation, enhancing antibiotic efficacy in a manner largely dependent on neutrophils. In contrast, NSG mice failed to potentiate tobramycin bacterial killing to increase PAMPs and mount Tobramycin-induced boost in immune activation, resulting in reduced infection control. Importantly, topical PAMPs (LPS and N-formyl-methionyl-leucyl-phenylalanine (fMLP)) restored immune activation and improved infection control in NSG mice in a manner that was also dependent on neutrophil's function.ConclusionThese findings provide direct experimental evidence that antibiotic efficacy requires synergy with host immunity. They highlight the therapeutic potential of augmenting innate immune activation to improve infection outcomes, particularly in immunocompromised patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41646972 · DOI · PMC12868242
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management [4]
- Research article Doxorubicin-An Agent with Multiple Mechanisms of Anticancer Activity [5]
- Research article Addition of gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia: a meta-analysis of individual patient data from randomised controlled trials [6]
- Research article Underlying the Mechanisms of Doxorubicin-Induced Acute Cardiotoxicity: Oxidative Stress and Cell Death [7]
- Research article Review and meta-analysis of incidence and clinical predictors of anthracycline cardiotoxicity [8]
- Research article Beta lactam monotherapy versus beta lactam-aminoglycoside combination therapy for sepsis in immunocompetent patients: systematic review and meta-analysis of randomised trials [9]
References
- Korkut Celikates B, Ilgin S, Yilmaz MU, Atli Eklioglu O. Targeting the powerhouse: the mitochondrial perspective on gentamicin-induced kidney injury. . 2026. PMID 41654647 · DOI · PMC13086777
- Collings H, Stone M, Chrysostomou M, Hirst A, Waldenberg TE, Yucel E, et al.. A systematic literature review and (network) meta-analysis of the effectiveness of ceftolozane/tazobactam versus aminoglycosides/polymyxins and ceftazidime/avibactam for treating adult patients with multidrug-resistant Pseudomonas aeruginosa infections. . 2026. PMID 41532768 · DOI · PMC12888884
- Padmakumari RG, Roy R, Mahmud F, Dehari D, Tesfaw G, Thomas C, et al.. Synergy between immune system and antibiotics drives infection control in mice. . 2025. PMID 41646972 · DOI · PMC12868242
- Rawat PS, Jaiswal A, Khurana A, Bhatti JS, Navik U. Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management. Biomed Pharmacother. 2021. PMID 34243633 · DOI
- Kciuk M, Gielecińska A, Mujwar S, Kołat D, Kałuzińska-Kołat Ż, Celik I, et al.. Doxorubicin-An Agent with Multiple Mechanisms of Anticancer Activity. Cells. 2023. PMID 36831326 · DOI · PMC9954613
- Hills RK, Castaigne S, Appelbaum FR, Delaunay J, Petersdorf S, Othus M, et al.. Addition of gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia: a meta-analysis of individual patient data from randomised controlled trials. Lancet Oncol. 2014. PMID 25008258 · DOI · PMC4137593
- Kong CY, Guo Z, Song P, Zhang X, Yuan YP, Teng T, et al.. Underlying the Mechanisms of Doxorubicin-Induced Acute Cardiotoxicity: Oxidative Stress and Cell Death. Int J Biol Sci. 2022. PMID 35002523 · DOI · PMC8741835
- Lotrionte M, Biondi-Zoccai G, Abbate A, Lanzetta G, D'Ascenzo F, Malavasi V, et al.. Review and meta-analysis of incidence and clinical predictors of anthracycline cardiotoxicity. Am J Cardiol. 2013. PMID 24075281 · DOI
- Paul M, Benuri-Silbiger I, Soares-Weiser K, Leibovici L. Beta lactam monotherapy versus beta lactam-aminoglycoside combination therapy for sepsis in immunocompetent patients: systematic review and meta-analysis of randomised trials. BMJ. 2004. PMID 14996699 · DOI · PMC381218
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.