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Proteogenomic integration reveals CXCL10 as a potentially downstream causal mediator for IL-6 signaling on atherosclerosis.
medRxiv
0
2023
CAD, CXCL10, IL-6, IL-6 receptor, IL-6R, LAAS, PAD, atheroprogression, atheroprotection, atherosclerosis, atherosclerotic lesions, cardiovascular, cardiovascular disease, coronary artery disease, human, immune cell, interferon, interleukin-6, large artery atherosclerotic stroke, peripheral artery disease
Author NameAffiliation
Barbara ThorandInstitute of Epidemiology, German Research Center for Environmental Health (GmbH)
Rainer MalikInstitute for Stroke and Dementia Research, Ludwig-Maximilians-University of Munich
Christian HerderGerman Center for Diabetes Research
Christian HerderMedical Faculty and University Hospital, Heinrich Heine University
Christian HerderInstitute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University
Annette PetersInstitute of Epidemiology, German Research Center for Environmental Health (GmbH)
Annette PetersGerman Center for Cardiovascular Health (DZHK e.V.
Annette PetersInstitute for Medical Information Processing, Ludwig-Maximilians-University Munich
Annette PetersInstitute of Epidemiology, German Research Center for Environmental Health (GmbH)
Annette PetersInstitute for Medical Information Processing, Ludwig-Maximilians-University Munich
Annette PetersGerman Center for Cardiovascular Health (DZHK e.V.
Aroon D HingoraniUniversity College London
Aroon D HingoraniInstitute of Cardiovascular Science, University College London
Jonathan RosandCenter for Genomic Medicine, Massachusetts General Hospital
Jonathan RosandBroad Institute of MIT and Harvard
Jonathan RosandHenry and Allison McCance Center for Brain Health, Massachusetts General Hospital
Jonathan RosandCenter for Genomic Medicine, Massachusetts General Hospital
Jonathan RosandBroad Institute of MIT and Harvard
Jonathan RosandHenry and Allison McCance Center for Brain Health, Massachusetts General Hospital
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