{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T04:49:07Z","timestamp":1787806147009,"version":"build-2784847793"},"reference-count":75,"publisher":"American Society for Clinical Investigation","issue":"20","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,12,8]]},"abstract":"<jats:p>\n                    Pentraxin-2 (PTX-2), also known as serum amyloid P component (SAP\/APCS), is a constitutive, antiinflammatory, innate immune plasma protein whose circulating level is decreased in chronic human fibrotic diseases. Here we show that recombinant human PTX-2 (rhPTX-2) retards progression of chronic kidney disease in\n                    <jats:italic>Col4a3<\/jats:italic>\n                    mutant mice with Alport syndrome, reducing blood markers of kidney failure, enhancing lifespan by 20%, and improving histological signs of disease. Exogenously delivered rhPTX-2 was detected in macrophages but also in tubular epithelial cells, where it counteracted macrophage activation and was cytoprotective for the epithelium. Computational analysis of genes regulated by rhPTX-2 identified the transcriptional regulator c-Jun along with its activator protein\u20131 (AP-1) binding partners as a central target for the function of rhPTX-2. Accordingly, PTX-2 attenuates c-Jun and AP-1 activity, and reduces expression of AP-1\u2013dependent inflammatory genes in both monocytes and epithelium. Our studies therefore identify rhPTX-2 as a potential therapy for chronic fibrotic disease of the kidney and an important inhibitor of pathological c-Jun signaling in this setting.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.87446","type":"journal-article","created":{"date-parts":[[2016,12,7]],"date-time":"2016-12-07T11:00:58Z","timestamp":1481108458000},"source":"Crossref","is-referenced-by-count":59,"title":["Pentraxin-2 suppresses c-Jun\/AP-1 signaling to inhibit progressive fibrotic disease"],"prefix":"10.1172","volume":"1","author":[{"given":"Naoki","family":"Nakagawa","sequence":"first","affiliation":[{"name":"Division of Nephrology, Departments of Medicine and Pathology, and"},{"name":"Institute of Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, USA."},{"name":"Department of Internal Medicine, Asahikawa Medical University, Asahikawa, 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