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Cardiac tissue acetylcholine (ACh) and serum ACh, tumour necrosis factor \u03b1 (TNF-\u03b1), interleukin 1\u03b2 (IL-1\u03b2) and interleukin 6 (IL-6) levels were detected by ELISA to determine whether VNS was successful. An inflammatory injury model in human coronary artery endothelial cells (HCAECs) was established by lipopolysaccharide and identified by evaluating TNF-\u03b1, IL-1\u03b2 and IL-6 levels and tube formation. Immunohistochemistry staining was performed to evaluate CD31-positive vessel density and stromal cell-derived factor-l alpha (SDF-1\u03b1) expression in the MI heart in vivo and the expression and distribution of SDF-1\u03b1, C-X-C motif chemokine receptor 4 and CXCR7 in HCAECs in vitro. Western blotting was used to detect the levels of SDF-1\u03b1, V-akt murine thymoma viral oncogene homolog (AKT), phosphorylated AKT (pAKT), specificity protein 1 (Sp1) and phosphorylation of Sp1 in HCAECs. Left ventricular performance, including left ventricular systolic pressure, left ventricular end-diastolic pressure and rate of the rise and fall of ventricular pressure, should be evaluated 28 days after VNS treatment. VNS was successfully established for MI therapy with decreases in serum TNF-\u03b1, IL-1\u03b2 and IL-6 levels and increases in cardiac tissue and serum ACh levels, leading to increased SDF-1\u03b1 expression in coronary endothelial cells of MI hearts, triggering angiogenesis of MI hearts with increased CD31-positive vessel density, which was abolished by the m\/nAChR inhibitors mecamylamine and atropine or knockdown of SDF-1\u03b1 by shRNA. ACh promoted SDF-1\u03b1 expression and its distribution along with the branch of the formed tube in HCAECs, resulting in an increase in the number of tubes formed in HCAECs. ACh increased the levels of pAKT and phosphorylation of Sp1 in HCAECs, resulting in inducing SDF-1\u03b1 expression, and the specific effects could be abolished by mecamylamine, atropine, the PI3K\/AKT blocker wortmannin or the Sp1 blocker mithramycin. Functionally, VNS improved left ventricular performance, which could be abolished by Ad-shSDF-1\u03b1.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>VNS promoted angiogenesis to repair the infarcted heart by inducing SDF-1\u03b1 expression and redistribution along new branches during angiogenesis, which was associated with the m\/nAChR-AKT-Sp1 signalling pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.14475","type":"journal-article","created":{"date-parts":[[2023,8,29]],"date-time":"2023-08-29T03:06:40Z","timestamp":1693278400000},"page":"3311-3329","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Vagus Nerve Stimulation-Induced Stromal Cell-Derived Factor-L Alpha Participates in Angiogenesis and Repair of Infarcted Hearts"],"prefix":"10.1093","volume":"10","author":[{"given":"Yan","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Physiology, Faculty of Basic Medical Sciences, Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei University of Medicine , Shiyan ,","place":["PR China"]},{"name":"Department of Pathology, Renmin Hospital, Hubei University of Medicine , Shiyan ,","place":["PR China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Physiology, Faculty of Basic Medical Sciences, Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei University of Medicine , Shiyan ,","place":["PR China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xing-yuan","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Physiology, Faculty of Basic Medical Sciences, Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei University of 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