ArticleFrontiers in physiology2021
Renal Inflammation and Innate Immune Activation Underlie the Transition From Gentamicin-Induced Acute Kidney Injury to Renal Fibrosis.
Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Repeated aminoglycoside exposure activates interferon-stimulated genes in human renal proximal tubular models.Archives of toxicology · 2026Article
- Caloric Restriction Attenuates Gentamicin-Induced Acute Kidney Injury and Is Associated with Changes in Oxidative Stress and Mitochondrial DNA Damage.Antioxidants (Basel, Switzerland) · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Amelioration of gentamicin-induced acute kidney injury by trifluoperazine: in vivo mechanistic insights.Scientific reports · 2026Article
- Erythropoietin alleviate obstructive renal fibrosis by regulating immunity and inflammation through miR-21-5p/SPRY1/ERK1/2/NF-κB pathway inhibition.Frontiers in molecular biosciences · 2026Article
- Protective effects of taxifolin against gentamicin-induced nephrotoxicity in mice: modulation of oxidative stress, inflammation, apoptosis, and Nrf2 signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Article
- Hypovitaminosis D Does Not Aggravate the Progression of Gentamicin-Induced Kidney Injury in Rats.Diseases (Basel, Switzerland) · 2025Article
- Ergosterol Protects Canine MDCK Cells from Gentamicin-Induced Damage by Modulating Autophagy and Apoptosis.Metabolites · 2025Article
- Natural antifibrosis potential of anthocyanin inResults in chemistry · 2025Article
- Verbenone prevents cyclophosphamide-induced oxidative stress, inflammation, fibrosis, and cellular changes in the kidneys of Swiss albino mice by targeting NF-ĸB/TGF-β signaling pathways.Iranian journal of basic medical sciences · 2025Article
- Bibliometric and visual analysis of immunisation associated with acute kidney injury from 2003 to 2023.Frontiers in pharmacology · 2024Article
- Oral delivery of nerolidol alleviates cyclophosphamide-induced renal inflammation, apoptosis, and fibrosis via modulation of NF-κB/cleaved caspase-3/TGF-β signaling molecules.Drug delivery · 2023Article
- From Physiology to Pathology: The Role of Mitochondria in Acute Kidney Injuries and Chronic Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- Formononetin Ameliorates Renal Dysfunction, Oxidative Stress, Inflammation, and Apoptosis and Upregulates Nrf2/HO-1 Signaling in a Rat Model of Gentamicin-Induced Nephrotoxicity.Frontiers in pharmacology · 2022Article
- Understanding the Renal Fibrotic Process in Leptospirosis.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subjects recovering from acute kidney injury (AKI) are at risk of developing chronic kidney disease (CKD). The mechanisms underlying this transition are unclear and may involve sustained activation of renal innate immunity, with resulting renal inflammation and fibrosis. We investigated whether the NF-κB system and/or the NLRP3 inflammasome pathway remain activated after the resolution of AKI induced by gentamicin (GT) treatment, thus favoring the development of CKD. Male Munich-Wistar rats received daily subcutaneous injections of GT, 80 mg/kg, for 9 days. Control rats received vehicle only (NC). Rats were studied at 1, 30, and 180 days after GT treatment was ceased. On Day 1, glomerular ischemia (ISCH), tubular necrosis, albuminuria, creatinine retention, and tubular dysfunction were noted, in association with prominent renal infiltration by macrophages and myofibroblasts, along with increased renal abundance of TLR4, IL-6, and IL1β. Regression of functional and structural changes occurred on Day 30. However, the renal content of IL-1β was still elevated at this time, while the local renin-angiotensin system remained activated, and interstitial fibrosis became evident. On Day 180, recurring albuminuria and mild glomerulosclerosis were seen, along with ISCH and unabated interstitial fibrosis, whereas macrophage infiltration was still evident. GT-induced AKI activates innate immunity and promotes renal inflammation. Persistence of these abnormalities provides a plausible explanation for the transition of AKI to CKD observed in a growing number of patients.
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