{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T23:39:16Z","timestamp":1793230756749,"version":"4.5.0"},"reference-count":38,"publisher":"American Society for Clinical Investigation","issue":"21","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,11,2]]},"abstract":"<jats:p>\n                    TGF-\u03b2 signals through a receptor complex composed of 2 type I and 2 type II (TGF-\u03b2RII) subunits. We investigated the role of macrophage TGF-\u03b2 signaling in fibrosis after AKI in mice with selective monocyte\/macrophage TGF-\u03b2RII deletion (macrophage TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice). Four weeks after injury, renal TGF-\u03b21 expression and fibrosis were higher in WT mice than macrophage TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice, which had decreased renal macrophages. The in vitro chemotactic response to f-Met-Leu-Phe was comparable between bone marrow\u2013derived monocytes (BMMs) from WT and macrophage TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice, but TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    BMMs did not respond to TGF-\u03b2. We then implanted Matrigel plugs suffused with either f-Met-Leu-Phe or TGF-\u03b21 into WT or macrophage TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice. After 6 days, f-Met-Leu-Phe induced similar macrophage infiltration into the Matrigel plugs of WT and macrophage TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice, but TGF-\u03b2 induced infiltration only in WT mice. We further determined the number of labeled WT or TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    BMMs infiltrating into WT kidneys 20 days after ischemic injury. There were more labeled WT BMMs than TGF-\u03b2RII\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    BMMs. Therefore, macrophage TGF-\u03b2RII deletion protects against the development of tubulointerstitial fibrosis following severe ischemic renal injury. Chemoattraction of macrophages to the injured kidney through a TGF-\u03b2\/TGF-\u03b2RII axis is a heretofore undescribed mechanism by which TGF-\u03b2 can mediate renal fibrosis during progressive renal injury.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.123563","type":"journal-article","created":{"date-parts":[[2018,11,1]],"date-time":"2018-11-01T11:01:23Z","timestamp":1541070083000},"source":"Crossref","is-referenced-by-count":119,"title":["TGF-\u03b2 promotes fibrosis after severe acute kidney injury by enhancing renal macrophage infiltration"],"prefix":"10.1172","volume":"3","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9886-8339","authenticated-orcid":true,"given":"Sungjin","family":"Chung","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA."},{"name":"Vanderbilt Center for Kidney Disease, Vanderbilt University School of Medicine, Nashville, Tennessee, USA."},{"name":"Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica M.","family":"Overstreet","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA."},{"name":"Vanderbilt Center for Kidney Disease, Vanderbilt University School of Medicine, Nashville, Tennessee, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA."},{"name":"Vanderbilt Center for Kidney Disease, Vanderbilt University School of Medicine, Nashville, Tennessee, 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