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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Oxidative stress–induced cell death, including DNA damage and ferroptosis, plays a critical role in both acute and chronic kidney injury. In particular, ischemia-reperfusion injury (IRI) and unilateral ureteral obstruction (UUO) are key models in which these mechanisms contribute to tubular cell death and renal fibrosis. 2-Mercaptoethanol (2-ME), an antioxidant and modulator of cysteine metabolism, protects against DNA double-strand breaks in bovine embryos and inhibits ferroptosis by promoting SLC7A11-dependent cysteine uptake in vitro. These findings suggest its potential to target multiple pathways involved in kidney injury. We investigated the protective effects and mechanisms of 2-ME in murine models of IRI and UUO.
The study involved inducing kidney IRI or performing a sham operation on mice. The mice were then treated with 2-ME and/or Ras-selective lethal 3 (RSL3), a potent inhibitor of glutathione peroxidase 4 (GPX4). Additionally, UUO or a sham operation was performed on the left kidneys of female mice, which were treated with 2-ME or vehicle control.
In the IRI model, 2-ME treatment significantly reduced kidney dysfunction, tubular injury, and DNA double-strand breaks. 2-ME enhanced the phosphorylation of ataxia telangiectasia mutated (ATM) and its downstream effectors, indicating activation of the ATM-mediated DNA damage response (DDR) pathway. Additionally, 2-ME markedly upregulated GPX4 expression. Inhibition of GPX4 exacerbated IRI-induced kidney dysfunction, tubular injury, and DNA double-strand breaks, while also impairing the activation of the ATM-mediated DDR signaling pathway in 2-ME-treated kidneys. In the UUO model, which induces ferroptosis and inflammation leading to fibrosis, pre-treatment with 2-ME restored the expression of antioxidant enzymes, reduced markers of ferroptosis, and suppressed inflammatory cytokines. However, 2-ME did not prevent the upregulation of fibrosis markers such as α-smooth muscle actin (α-SMA) and collagen genes. Therapeutic treatment with 2-ME showed no significant effect on ferroptosis regulation, oxidative stress, inflammation, or fibrosis compared to vehicle treatment.
Collectively, our findings demonstrate that pre-treatment with 2-ME protects against kidney injury through distinct mechanisms: by activating DDR signaling and antioxidant defenses in IRI, and by inhibiting ferroptosis and inflammation in UUO. These results highlight the therapeutic potential of 2-ME in modulating multiple injury pathways in the kidney.
