{"database":"bioimages","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":[null],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-BIAD1635"],"repository":["bioimages"],"figure_sub":["Specimen","Image analysis","Study Component","organisation","Biosample","Associations","Image acquisition"],"pubmed_authors":["Mauro Perretti "],"additional_accession":[]},"is_claimable":false,"name":"Formyl-peptide receptor type 2 activation mitigates secondary organ damage in inflammatory arthritis EMM-2024-20382\n","description":"Rheumatoid arthritis (RA) is associated with heart and lung dysfunction. Current therapies\nfail to attenuate such complications. Here, we identify formyl-peptide receptor type 2 (FPR2)\nas therapeutic target to treat heart and lung dysfunction associated with inflammatory arthritis.\nArthritic mice on high levels of dietary homocysteine develop cardiac diastolic dysfunction\nand reduced lung compliance, mirroring two comorbidities in RA. Therapeutic administration\nof a small molecule FPR2 agonist (BMS986235) to hyper-homocysteine arthritic mice\nprevented diastolic dysfunction (monitored by echocardiography) and restored lung\ncompliance. These tissue-specific effects were secondary to reduced neutrophil infiltration,\nmodulation of fibroblast activation and phenotype (in the heart) and attenuat","dates":{"release":"2025-02-13T00:00:00Z","modification":"2025-02-13T11:29:59.73Z","creation":"2025-02-13T11:29:59.73Z"},"accession":"S-BIAD1635","cross_references":{}}