{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:59:44Z","timestamp":1790873984845,"version":"4.1.0"},"reference-count":54,"publisher":"Ovid Technologies (Wolters Kluwer Health)","funder":[{"DOI":"10.13039\/spng2nrbmu1l","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK108803"],"award-info":[{"award-number":["R01DK108803"]}],"id":[{"id":"10.13039\/spng2nrbmu1l","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/splg8urz3uzt","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["U01DK133081, U01DK133091, U01DK133092, U01DK133093, U01DK133095, U01DK133097, U01DK114866, U01DK114908, U01DK133090, U01DK133113, U01DK133766, U01DK133768, U01DK114907, U01DK114920, U01DK114923, U01DK114933, U24DK114886, UH3DK114926, UH3DK114861, UH3DK114915, UH3DK114937"],"award-info":[{"award-number":["U01DK133081, U01DK133091, U01DK133092, U01DK133093, U01DK133095, U01DK133097, U01DK114866, U01DK114908, U01DK133090, U01DK133113, U01DK133766, U01DK133768, U01DK114907, U01DK114920, U01DK114923, U01DK114933, U24DK114886, UH3DK114926, UH3DK114861, UH3DK114915, UH3DK114937"]}],"id":[{"id":"10.13039\/splg8urz3uzt","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["CJASN"],"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>The ephrin\u2013Eph signaling pathway emerged as the strongest blood proteomic correlate of interstitial fibrosis and tubular atrophy burden in a biopsy-confirmed diabetic kidney disease cohort.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This association was independently validated in 2 external multiethnic cohorts and was associated with a higher risk of subsequent kidney failure.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Kidney multiome analyses linked ephrin\u2013Eph signaling to intrarenal epithelial\u2013mesenchymal transition\u2013related molecular programs in diabetic kidney.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Diabetic kidney disease (DKD) is characterized by heterogeneous renal histological patterns, among which interstitial fibrosis and tubular atrophy (IFTA) is a key determinant of patient outcomes and treatment response. However, blood biomarkers reflecting IFTA burden remain unestablished.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We conducted SomaScan-based blood proteomic profiling in Korean patients with biopsy-confirmed diabetic nephropathy from the Seoul National University Hospital (\n                      <jats:italic toggle=\"yes\">n<\/jats:italic>\n                      =129). Linear regression analyses were used to identify pathways associated with IFTA area, and those additionally upregulated compared with healthy individuals were prioritized. Findings were validated in 2 external cohorts with available SomaScan data and histologic IFTA assessment: the Kidney Precision Medicine Project (KPMP;\n                      <jats:italic toggle=\"yes\">n<\/jats:italic>\n                      =73) and the Boston Kidney Biopsy Cohort (\n                      <jats:italic toggle=\"yes\">n<\/jats:italic>\n                      =414). Renal expression and downstream signaling of pathway components were evaluated using human kidney multiome data from KPMP.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In the diabetic nephropathy from Seoul National University Hospital cohort, the ephrin receptor signaling pathway emerged as the top pathway both positively associated with IFTA area and upregulated in patients with DKD. This association was replicated in the KPMP and Boston Kidney Biopsy Cohort cohorts. High activity of the ephrin receptor signaling pathway was also associated with a higher risk of kidney failure. Kidney tissue analyses demonstrated a higher expression of ephrin\u2013Eph signaling components, particularly genes encoding EPHA4 and EPHB1, in diabetic kidneys. Renal expression of these genes correlated with epithelial\u2013mesenchymal transition signatures, accompanied by downstream activation of hypoxia, Janus kinase\u2013signal transducer and activator of transcription, and TGF\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      signaling pathways across multiple kidney cell types.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Upregulation of the ephrin receptor signaling pathway represents a robust and reproducible blood proteomic signature reflecting IFTA in DKD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2215\/cjn.0000001191","type":"journal-article","created":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T16:00:21Z","timestamp":1787328021000},"update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Circulating Ephrin\u2013Eph Signaling Reflects Interstitial Fibrosis and Tubular Atrophy in Diabetic Kidney Disease"],"prefix":"10.2215","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0137-5261","authenticated-orcid":false,"given":"Seung Seok","family":"Han","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Mass General Brigham, Boston, Massachusetts"},{"name":"Endocrine Unit, Department of Medicine, Mass General Brigham, Boston, Massachusetts"},{"name":"Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 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Seoul, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-8553-1853","authenticated-orcid":false,"given":"Xufan","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Medicine, New York University Grossman School of Medicine, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1969-8360","authenticated-orcid":false,"given":"Kyung Chul","family":"Moon","sequence":"additional","affiliation":[{"name":"Department of Pathology, Seoul National University College of Medicine, Seoul, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8109-1420","authenticated-orcid":false,"given":"Anand","family":"Srivastava","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Illinois Chicago, Chicago, 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