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ArticleVolume 38, Issue 8p1599-1617.e8Open access Affiliations & Notes 1University of Michigan, Department of Molecular & Integrative Physiology, Ann Arbor, MI, United States of America 2University of Michigan, Department of Biological Chemistry, Ann Arbor, MI, United States of America 3University of Michigan, Program in Cellular and Molecular Biology, Ann Arbor, MI, United States of America 4Medical Scientist Training Program, University of Michigan, Ann Arbor, MI, 48109, United States of...
Abstract Increased reactive oxygen species (ROS) levels are a hallmark of inflammatory bowel disease (IBD) and constitute a major mechanism of epithelial cell death. Approaches to broadly inhibit ROS have had limited efficacy in treating IBD. Here we show that lipid peroxidation contributes to the pathophysiology of IBD by promoting ferroptosis, an iron-dependent form of programmed cell death.
Abstract Effective therapies are lacking for patients with advanced colorectal cancer (CRC). The CRC tumor microenvironment has elevated metabolic waste products due to altered metabolism and proximity to the microbiota. The role of metabolite waste in tumor development, progression, and treatment resistance is unclear. We generated an autochthonous metastatic mouse model of CRC and used unbiased multi-omic analyses to reveal a robust accumulation of tumoral ammonia.
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