{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Michailidou D"],"funding":["NHLBI NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["e70021"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11897803"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(3)"],"pubmed_abstract":["<h4>Objective</h4>Platelet activation is thought to participate in polymyalgia rheumatica (PMR) pathogenesis. Upon platelet activation, mitochondria are expelled into the extracellular space. However, whether extracellular mitochondria are present in patients with PMR and whether they can induce platelet activation is not known.<h4>Methods</h4>To investigate this, we measured markers of platelet activation (thrombospondin-1 [TSP-1]), mitochondrial-derived N-formyl methionine peptide (fMET), and autoantibodies directed toward specific mitochondrial antigen mitofusin-1 (MFN1) by enzyme-linked immunosorbent assay in plasma of healthy controls (HCs, n = 30) and patients with PMR without giant cell arteritis (GCA) (n = 45) and patients with PMR with GCA (n = 9) before and after treatment with g"],"journal":["ACR open rheumatology"],"pubmed_title":["Mitochondrial-Mediated Platelet Activation in Polymyalgia Rheumatica."],"pmcid":["PMC11897803"],"funding_grant_id":["#5T32HL007028-44","#5T32HL007028‐44","1R21-EY-029391","T32 HL007028","1R21‐EY‐029391","R21AR075129","1R01HL158606"],"pubmed_authors":["Michailidou D","Chen J","Lopez JA","Wang T","Chapa JAG","Lood C","Rantapaa-Dahlqvist S","Johansson L"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial-Mediated Platelet Activation in Polymyalgia Rheumatica.","description":"<h4>Objective</h4>Platelet activation is thought to participate in polymyalgia rheumatica (PMR) pathogenesis. Upon platelet activation, mitochondria are expelled into the extracellular space. However, whether extracellular mitochondria are present in patients with PMR and whether they can induce platelet activation is not known.<h4>Methods</h4>To investigate this, we measured markers of platelet activation (thrombospondin-1 [TSP-1]), mitochondrial-derived N-formyl methionine peptide (fMET), and autoantibodies directed toward specific mitochondrial antigen mitofusin-1 (MFN1) by enzyme-linked immunosorbent assay in plasma of healthy controls (HCs, n = 30) and patients with PMR without giant cell arteritis (GCA) (n = 45) and patients with PMR with GCA (n = 9) before and after treatment with g","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-06-25T03:04:15.329Z","creation":"2025-04-04T01:29:27.184Z"},"accession":"S-EPMC11897803","cross_references":{"pubmed":["40071558"],"doi":["10.1002/acr2.70021"]}}