{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T20:48:01Z","timestamp":1791233281936,"version":"4.1.0"},"reference-count":36,"publisher":"American Diabetes Association","issue":"6","license":[{"start":{"date-parts":[[2025,2,27]],"date-time":"2025-02-27T00:00:00Z","timestamp":1740614400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"DOI":"10.13039\/501100001711","name":"Schweizerischer Nationalfonds zur Forderung der Wissenschaftlichen Forschung","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,6,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Revascularization strategies failed to improve outcome in patients with diabetes with peripheral artery disease (PAD). Histone modifications are key modulators of gene expression and could play a role in angiogenic response. This study investigates the role of chromatin remodelling in modulating angiogenesis in diabetes. RNA sequencing (RNA-seq), and angiogenic assays (cell migration and tube formation) were performed in human aortic endothelial cells (HAECs) exposed to normal glucose (NG, 5 mmol\/L) or high glucose (HG, 25 mmol\/L) for 48 h. The expression of the histone methyltransferase SETD7 and its chromatin signature at histone 3 on lysine 4 (H3K4me1) were investigated by Western blot and chromatin immunoprecipitation (ChIP). Diabetic mice were treated with the SETD7 inhibitor (R)-PFI-2 or vehicle and underwent hind limb ischemia by femoral artery ligation. The experimental findings were translated into two cohorts of patients with diabetes with PAD. RNA-seq in HG-treated HAECs unveiled SETD7 as the top-ranking transcript. SETD7 upregulation was associated with increased H3K4me1 levels and defective angiogenesis. Both SETD7 depletion and (R)-PFI-2 rescued hyperglycemia-induced impairment of HAECs migration and tube formation, while SETD7 overexpression blunted the angiogenic response. RNA-seq and ChIP assays showed that SETD7-induced H3K4me1 enables the transcription of the angiogenesis inhibitor semaphorin-3G (SEMA3G) by increasing chromatin accessibility to peroxisome proliferator\u2013activated receptor-\u03b3. In diabetic mice with hind limb ischemia, (R)-PFI-2 improved limb perfusion by suppressing SEMA3G. The SETD7\/SEMA3G axis was upregulated in patients with diabetes with PAD. Of note, (R)-PFI-2 restored angiogenic properties in endothelial cells collected from patients with diabetes. These findings show that SETD7 is a druggable epigenetic target in diabetic PAD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>Hyperglycemia increases SETD7 expression and SETD7-dependent histone 3 on lysine 4, thus leading to an open chromatin and active transcription of the antiangiogenic gene semaphorin-3G (SEMA3G). Gene silencing and selective pharmacological inhibition of SETD7 by (R)-PFI-2 both blunt histone 3 on lysine 4 levels and SEMA3G transcription, thus rescuing hyperglycemia-induced impairment of angiogenic properties. The SETD7 inhibitor (R)-PFI-2 promotes neovascularization and restores limb perfusion in diabetic mice. SETD7\/SEMA3G signaling was dysregulated in two different cohorts of patients with diabetes with peripheral arterial disease. Treatment with (R)-PFI-2 in endothelial cells collected from patients with diabetes restores angiogenic properties.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db24-0997","type":"journal-article","created":{"date-parts":[[2025,2,27]],"date-time":"2025-02-27T10:42:18Z","timestamp":1740652938000},"page":"969-982","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":17,"title":["Targeting SETD7 Rescues Diabetes-Induced Impairment of Angiogenic Response by Transcriptional Repression of Semaphorin-3G"],"prefix":"10.2337","volume":"74","author":[{"given":"Shafeeq A.","family":"Mohammed","sequence":"first","affiliation":[{"name":"1Department of Cardiology, Center for Translational and Experimental Cardiology (CTEC), Zurich University Hospital and University of Z\u00fcrich, Schlieren, 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Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandro","family":"Mengozzi","sequence":"additional","affiliation":[{"name":"1Department of Cardiology, Center for Translational and Experimental Cardiology (CTEC), Zurich University Hospital and University of Z\u00fcrich, Schlieren, Switzerland"},{"name":"5Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy"},{"name":"6Health Science Interdisciplinary Center, Sant\u2019Anna School of Advanced Studies, Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlo Maria","family":"Caravaggi","sequence":"additional","affiliation":[{"name":"7Diabetic Foot Department, IRCCS MultiMedica, Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samuele","family":"Ambrosini","sequence":"additional","affiliation":[{"name":"1Department of Cardiology, Center for Translational and Experimental Cardiology (CTEC), Zurich University Hospital and University of Z\u00fcrich, Schlieren, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefano","family":"Masi","sequence":"additional","affiliation":[{"name":"5Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy"},{"name":"8Institute of Cardiovascular Science, University College London, London, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Cristina","family":"Vinci","sequence":"additional","affiliation":[{"name":"9Unit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino IRCCS, Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Omer","family":"Dzemali","sequence":"additional","affiliation":[{"name":"1Department of Cardiology, Center for Translational and Experimental Cardiology (CTEC), Zurich University Hospital and University of Z\u00fcrich, Schlieren, Switzerland"},{"name":"10Department of Cardiac Surgery, University Hospital Zurich, Zurich, Switzerland"},{"name":"11Department of Cardiac Surgery, Zurich City Hospital-Triemli, Zurich, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7996-6809","authenticated-orcid":false,"given":"Gaia","family":"Spinetti","sequence":"additional","affiliation":[{"name":"12Cardiovascular Pathophysiology-Regenerative Medicine Laboratory, IRCCS MultiMedica, Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjay","family":"Rajagopalan","sequence":"additional","affiliation":[{"name":"13Harrington Heart and Vascular Institute, University Hospitals, Cleveland, OH"},{"name":"14Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7968-7375","authenticated-orcid":false,"given":"Assam","family":"El-Osta","sequence":"additional","affiliation":[{"name":"15Epigenetics in Human 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