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We aimed to investigate whether modulation of the SNS through renal denervation (RDN) influences myocardial remodeling following MI. MI in rats was induced 2 days after bilateral RDN or Sham surgery. Cardiac MRI showed that left ventricular ejection fraction was significantly higher in RDN-treated MI rats compared to Sham-treated MI rats. RNA sequencing of left ventricular tissue revealed that RDN suppresses fibrosis and inflammation related pathways at the whole transcriptome level, with clear separation of the experimental groups. These findings were confirmed by histochemical, gene, and protein expression analyses, which found a significantly higher extent of fibrosis and CD206 expression in the MI rats compared to RDN-treated MI rats. To simulate SNS activity, PMA-differentiated THP-1 cells were incubated with the \u03b2-adrenoceptor agonist isoprenaline. This resulted in upregulation of profibrotic macrophage gene expression, which was not the case after co-stimulation with a \u03b21-adrenoceptor antagonist. Modulation of the SNS through RDN mitigates left ventricular remodeling post-MI by reducing myocardial fibrosis and scar size. Heightened SNS activity promotes a profibrotic macrophage phenotype. These findings support investigation into the therapeutic potential of RDN for managing MI patients.<\/jats:p>","DOI":"10.1038\/s41598-026-50195-w","type":"journal-article","created":{"date-parts":[[2026,4,26]],"date-time":"2026-04-26T14:55:31Z","timestamp":1777215331000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Renal denervation attenuates cardiac fibrosis and improves left ventricular function in rats with myocardial infarction"],"prefix":"10.1038","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1884-5656","authenticated-orcid":false,"given":"Markus","family":"Therre","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mathias","family":"Hohl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Parisa","family":"Aghagolzadeh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simina-Ramona","family":"Selejan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucas","family":"Lauder","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mert","family":"Tokcan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philipp","family":"Markwirth","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald","family":"Engler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"H\u00fcbner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"M\u00fcller","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anh Khoa Dennis","family":"Huynh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Kahles","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mathias","family":"Konstandin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"B\u00f6hm","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix","family":"Mahfoud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,26]]},"reference":[{"key":"50195_CR1","doi-asserted-by":"publisher","first-page":"919","DOI":"10.1016\/S0008-6363(99)00139-X","volume":"43","author":"XJ Du","year":"1999","unstructured":"Du, X. 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MB is supported by the Deutsche Forschungsgemeinschaft (German Research Foundation; TTR 219, project number 322900939) and reports personal fees from Abbott, Amgen, Astra Zeneca, Bayer, Boehringer Ingelheim, Cytokinetics, Edwards, Medtronic, Novartis, Pharmacosmos, Recor, Servier and Vifor during the conduct of the study. FM is supported by Deutsche Gesellschaft f\u00fcr Kardiologie (DGK), Deutsche Forschungsgemeinschaft (SFB TRR219, Project-ID 322900939), and Deutsche Herzstiftung. Saarland University has received scientific support from Ablative Solutions, Medtronic and ReCor Medical. Until May 2024, FM has received speaker honoraria\/consulting fees from Ablative Solutions, Amgen, Astra-Zeneca, Bayer, Boehringer Ingelheim, Inari, Medtronic, Merck, ReCor Medical, Servier, and Terumo. The other authors report no relationships relevant to the contents of this paper to disclose.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"13416"}}