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While oxidative stress is well recognized as a central pathogenic driver, the contribution of DNA damage resolution pathways to hepatocyte survival remains poorly defined. Here we report the development of a small molecule, CMM\u201098, that installs a robust AP\u2010site processing function in the DNA glycosylase OGG1 by binding the active site. Acting on the Schiff base intermediate, the molecule effectively rewires the enzyme's catalytic outcome under oxidative stress, boosting AP site turnover by 57\u2010fold. Using cellular and in vivo models of acetaminophen\u2010induced liver failure, we demonstrate that OGG1 catalysis manipulated by CMM\u201098 reduces oxidative DNA damage burden, promotes the resolution of oxidative DNA lesions, and ameliorates hepatocyte injury. These findings identify DNA repair capacity as a modifiable determinant of acute liver injury outcome and establish chemical switching of OGG1 as a strategy to support hepatocyte resilience under extreme oxidative stress.<\/jats:p>","DOI":"10.1002\/advs.77956","type":"journal-article","created":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T18:00:31Z","timestamp":1790532031000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Stimulation of OGG1 Enhances Oxidative DNA Damage Repair and Protects Against Acute Liver Failure by Acetaminophen"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1976-0790","authenticated-orcid":false,"given":"Zhenjun","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Liver Surgery Renji Hospital School of Medicine Shanghai Jiao Tong University  Shanghai 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