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Here, our study of an autopsy cohort of patients with COVID-19 provided evidence that injury of TECs by myoglobin, released as a consequence of rhabdomyolysis, is a major pathophysiological mechanism for AKI in severe COVID-19. Analyses of human kidney biopsies, mouse models of myoglobinuric and gentamicin-induced AKI, and mouse kidney tubuloids showed that TEC injury resulted in activation of the glucocorticoid receptor by endogenous glucocorticoids, which aggravated tubular damage. The detrimental effect of endogenous glucocorticoids on injured TECs was exacerbated by the administration of a widely clinically used synthetic glucocorticoid, dexamethasone, as indicated by experiments in mouse models of myoglobinuric- and folic acid\u2013induced AKI, human and mouse kidney tubuloids, and human kidney slice cultures. Mechanistically, studies in mouse models of AKI, mouse tubuloids, and human kidney slice cultures demonstrated that glucocorticoid receptor signaling in injured TECs orchestrated a maladaptive transcriptional program to hinder DNA repair, amplify injury-induced DNA double-strand break formation, and dampen mTOR activity and mitochondrial bioenergetics. This study identifies glucocorticoid receptor activation as a mechanism of epithelial maladaptation, which is functionally important for AKI.<\/jats:p>","DOI":"10.1126\/scitranslmed.adk5005","type":"journal-article","created":{"date-parts":[[2024,10,2]],"date-time":"2024-10-02T17:59:31Z","timestamp":1727891971000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":22,"title":["Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury"],"prefix":"10.1126","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1065-6604","authenticated-orcid":true,"given":"Luping","family":"Zhou","sequence":"first","affiliation":[{"name":"Institute of Pharmacology, University of Marburg, Karl-von-Frisch-Stra\u00dfe 2, Marburg 35043, Germany."},{"name":"Department of Endocrinology and Metabolism, Affiliated Hospital of Southwest Medical University, Taiping Street 25, Luzhou 646000, 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