{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu W"],"funding":["NHLBI NIH HHS","NCI NIH HHS"],"pagination":["572-586"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10399458"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["2(6)"],"pubmed_abstract":["Clonal hematopoiesis (CH) increases the risk of atherosclerotic cardiovascular disease possibly due to increased plaque inflammation. Human studies suggest that limitation of interleukin-6 (IL-6) signaling could be beneficial in people with large CH clones, particularly in <i>TET2</i> CH. Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by <i>Tet2</i> CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression. IL-6 induces expression of <i>Csf1r</i> in <i>Tet2</i>-deficient macrophages through enhanced STAT3 binding to its promoter. In mouse and human <i>Tet2</i>-deficient macrophages, IL-6 increases CSF1R expression and enhances macrophage survival. Treatment with the CSF1R in"],"journal":["Nature cardiovascular research"],"pubmed_title":["Blockade of IL-6 signaling alleviates atherosclerosis in <i>Tet2</i>-deficient clonal hematopoiesis."],"pmcid":["PMC10399458"],"funding_grant_id":["R01 HL148071","R01 HL118567","R01 HL163099","P30 CA008748","R01 HL155431","R01 HL134892","R35 HL145228"],"pubmed_authors":["Yalcinkaya M","Olszewska M","Papapetrou EP","Xiao T","Ampomah PB","Liu W","Vela PS","Levine R","Wang N","Tall AR","Tabas I","Wang R","Libby P","Maestre IF","Heimlich JB","Bick AG"],"additional_accession":[]},"is_claimable":false,"name":"Blockade of IL-6 signaling alleviates atherosclerosis in <i>Tet2</i>-deficient clonal hematopoiesis.","description":"Clonal hematopoiesis (CH) increases the risk of atherosclerotic cardiovascular disease possibly due to increased plaque inflammation. Human studies suggest that limitation of interleukin-6 (IL-6) signaling could be beneficial in people with large CH clones, particularly in <i>TET2</i> CH. Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by <i>Tet2</i> CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression. IL-6 induces expression of <i>Csf1r</i> in <i>Tet2</i>-deficient macrophages through enhanced STAT3 binding to its promoter. In mouse and human <i>Tet2</i>-deficient macrophages, IL-6 increases CSF1R expression and enhances macrophage survival. Treatment with the CSF1R in","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jun","modification":"2025-04-04T07:44:56.418Z","creation":"2025-04-04T07:44:56.418Z"},"accession":"S-EPMC10399458","cross_references":{"pubmed":["37539077"],"doi":["10.1038/s44161-023-00281-3"]}}