ArticleBiomolecules2026
Albumin Protects Against Cyclophosphamide-Induced Hemorrhagic Cystitis by Scavenging Acrolein and Reactive Oxygen Species.
Article in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Exploration and experimental validation of oxidative stress-related diagnostic genes in interstitial cystitis based on transcriptomics.Translational andrology and urology · 2026Article
- Biomaterials and Nanomedicine for Mucosal Repair and Inflammation Control in Interstitial Cystitis/Bladder Pain Syndrome: An Extensive Review.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclophosphamide (CYP) is an effective chemotherapeutic, but its use is limited by hemorrhagic cystitis caused by its toxic metabolite acrolein. Acrolein, when concentrated in the urine, triggers oxidative stress, leading to urothelial inflammation and cell death. Given that albumin is the most abundant plasma protein that contains free thiol groups capable of neutralizing electrophiles and oxidants, we, therefore, hypothesized that albumin could mitigate CYP-induced bladder injury. Here, we tested this hypothesis. In CYP-induced mouse cystitis, albumin administration markedly reduced bladder enlargement, edema, and hemorrhage, effectively normalizing the bladder weight. Albumin also reduced bladder oxidative injury and preserved the expression of anti-ferroptotic proteins, including the cystine/glutamate antiporter xCT and glutathione peroxidase 4 (GPX4). In addition, albumin-treated mice showed less leakage of inflammatory protein into bladder tissue. In vitro, albumin protected urothelial cells from acrolein-induced cell death. It also significantly prevented H
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Registered trials
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