{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T12:34:56Z","timestamp":1793277296527,"version":"4.5.0"},"reference-count":56,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:00:00Z","timestamp":1791936000000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004731","name":"Zhejiang Provincial Natural Science Foundation","doi-asserted-by":"publisher","award":["LQ22H020011"],"award-info":[{"award-number":["LQ22H020011"]}],"id":[{"id":"10.13039\/501100004731","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["FS\/17\/24\/32596"],"award-info":[{"award-number":["FS\/17\/24\/32596"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["PG\/15\/11\/31279"],"award-info":[{"award-number":["PG\/15\/11\/31279"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["PG\/15\/86\/31723"],"award-info":[{"award-number":["PG\/15\/86\/31723"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["PG\/20\/10458"],"award-info":[{"award-number":["PG\/20\/10458"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["PG\/23\/11371"],"award-info":[{"award-number":["PG\/23\/11371"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Vein graft (VG) failure due to adverse remodelling and aggressive neointimal hyperplasia is a major complication and key limiting factor for maintaining long-term VG patency. CD34+ cells have been implicated in multiple cardiovascular diseases, but their functional involvements and contributions to VG failure remain elusive. In this study, we aimed to investigate the functional role of CD34+ cells in VG pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and result<\/jats:title>\n                    <jats:p>Single-cell RNA sequencing (scRNA-seq) analysis was conducted to uncover cellular heterogeneity of normal healthy and grafted veins as well as CD34+ cells in VGs. Genetic lineage tracing and depletion strategies were applied to delineate the functional involvements and potential contributions of CD34+ cells to VG remodelling. Multiple functional and biochemistry assays were conducted to identify and elucidate the key signal pathways underpinning smooth muscle cell (SMC) ferroptosis and phenotype switching. A total of 22 513 cells from normal healthy and grafted veins were included in scRNA-seq analysis, which showed a heterogeneous population of CD34+ cells as well as activated ferroptosis pathways and SMC phenotypic alterations in VGs. Using the inducible lineage tracing Cd34-CreERT2;R26-tdTomato mouse model, we showed that CD34+ cells were mainly differentiated into fibroblasts in VGs. Depletion of CD34+\/Postn+ myofibroblasts in a triple transgenic (Cd34-Dre;Postn-CreERT2;Dou-tdT-DTR) mouse model significantly decreased VG-induced neointimal hyperplasia. Cellular communication analysis identified Jagged 1\/Notch3 (neurogenic locus notch homologue protein 3) as the most upregulated signalling axis between CD34+ cell-derived fibroblasts and SMCs. Notch3 activation in SMCs by CD34+ cell-derived fibroblasts promoted SMC ferroptosis and switching to a synthetic\/secretory phenotype in VGs. Blocking Jagged1 and Notch3 signalling as well as inhibition of ferroptosis attenuated vascular adverse remodelling and neointimal hyperplasia in VGs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study provides a transcriptional and cellular landscape in normal healthy and grafted veins and shows that heterogeneous CD34+ cells serve as a key contributor to vascular remodelling and neointimal hyperplasia in VGs. We also demonstrate that CD34+ cell-derived myofibroblasts promote neointimal hyperplasia through Jagged1\/Notch3 signal axis, suggesting that blocking Jagged1\/Notch3 activation or inhibiting ferroptosis may provide a novel approach to prevent VG failure.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvag235","type":"journal-article","created":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T10:33:49Z","timestamp":1791974029000},"source":"Crossref","is-referenced-by-count":0,"title":["CD34+ myofibroblasts promote neointima formation in vein grafts by activating ferroptosis-induced smooth muscle cell phenotype switch"],"prefix":"10.1093","author":[{"given":"Simon S","family":"Xu","sequence":"first","affiliation":[{"name":"Academic Department of Vascular Surgery, South Bank Section, School of Cardiovascular and Metabolic Medicine & Sciences, King\u2019s BHF Centre of Research Excellence, King\u2019s College London , 249 Westminster Bridge Road, London SE1 7EH 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,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaodong","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, the First Affiliated Hospital, Zhejiang University School of Medicine , 79 Qingchun Road, Hangzhou, Zhejiang 310003 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Cardiology, the First Affiliated Hospital, Zhejiang University School of Medicine , 79 Qingchun Road, Hangzhou, Zhejiang 310003 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashish","family":"Patel","sequence":"additional","affiliation":[{"name":"Academic Department of Vascular Surgery, South Bank Section, School of Cardiovascular and Metabolic Medicine & Sciences, King\u2019s BHF Centre of Research Excellence, King\u2019s College London , 249 Westminster Bridge Road, London SE1 7EH 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