{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Aroca-Crevillen A"],"funding":["China Scholarship Council","Cancer Research UK","Agence Nationale de la Recherche","NHLBI NIH HHS","National Institutes of Health","Centro Nacional de Investigaciones Cardiovasculares","La Caixa Foundation","Spanish State Research Agency","Pro-CNIC Foundation","Instituto de Salud Carlos III","European Union","Sociedad Española de Cardiología","Ministerio de Ciencia, Innovación y Universidades","Medical Research Council","Boehringer Ingelheim","Janssen","AstraZeneca","Fondation pour la Recherche Médicale","Leducq Trans-Atlantic Network of Excellence on Circadian Effects in Stroke","Wellcome Trust","NIH HHS","European Regional Development Fund"],"pagination":["e20250240"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7618653"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["223(2)"],"pubmed_abstract":["Inflammation-driven injury, a significant source of morbidity and mortality worldwide, is largely mediated by the cytotoxic activities of neutrophils, which extend the initial lesion and jeopardize organ function. Intriguingly, inflammatory injury naturally declines at specific times of day, suggesting that circadian mechanisms exist that mitigate the destructive activity of neutrophils and protect the host. Here, we show that the periods of diurnal protection coincide with peaks in plasma CXCL12, a chemokine that inhibits the neutrophil-intrinsic circadian clock by signaling through CXCR4. Genetic deletion of this clock, or a hyperactive form of CXCR4, prevented the diurnal spikes of injury, and treatment with a synthetic CXCR4 agonist conferred protection from myocardial and vascular inj"],"journal":["The Journal of experimental medicine"],"pubmed_title":["A circadian checkpoint relocates neutrophils to minimize injury."],"pmcid":["PMC7618653"],"funding_grant_id":["CC2273","HL069438","LCF/BQ/DR19/11740022","PRE2019-089130","PI21/01572","HL116340","TNE-21CVD04","ANR-17-CE14-0019","201606350089","HR17_00527","CEX2020-001041-S","R01 HL116340","EQU202203014627","R01 HL069438","LCF/BQ/DR21/11880022","EU4H-2022-JA-03","PID2022-140616OB-I00"],"pubmed_authors":["Ortiz-Perez JT","Martin-Salamanca S","Rubio-Ponce A","Hidalgo A","Rosillo N","Bachelerie F","Nicolaes GAF","Aroca-Crevillen A","Liu X","Crainiciuc G","Sicilia J","Moro MA","Torres LS","Penaloza-Martinez E","Molina-Moreno M","Nunez V","Wichapong K","Sancho D","Adrover JM","Vicanolo T","Balabanian K","Bueno H","Casanova-Acebes M"],"additional_accession":[]},"is_claimable":false,"name":"A circadian checkpoint relocates neutrophils to minimize injury.","description":"Inflammation-driven injury, a significant source of morbidity and mortality worldwide, is largely mediated by the cytotoxic activities of neutrophils, which extend the initial lesion and jeopardize organ function. Intriguingly, inflammatory injury naturally declines at specific times of day, suggesting that circadian mechanisms exist that mitigate the destructive activity of neutrophils and protect the host. Here, we show that the periods of diurnal protection coincide with peaks in plasma CXCL12, a chemokine that inhibits the neutrophil-intrinsic circadian clock by signaling through CXCR4. Genetic deletion of this clock, or a hyperactive form of CXCR4, prevented the diurnal spikes of injury, and treatment with a synthetic CXCR4 agonist conferred protection from myocardial and vascular inj","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-06-17T07:00:27.448Z","creation":"2026-06-17T03:10:24.926Z"},"accession":"S-EPMC7618653","cross_references":{"pubmed":["41385080"],"doi":["10.1084/jem.20250240"]}}