{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T04:14:24Z","timestamp":1792815264553,"version":"4.5.0"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,5,19]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Vascular calcification (VC), a pathological process driven by the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs), markedly increases cardiovascular mortality. Vericiguat, a soluble guanylate cyclase stimulator, has shown vascular protective properties, but its role in modulating VC remains poorly investigated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">VC models were generated using the nephrectomy method or an adenine diet. Calcification in rat VSMCs and aortic rings was induced by high phosphate. VC was evaluated by Alizarin Red staining, calcium quantification, alkaline phosphatase activity, and imaging. Transcriptomic profiling and viral vector approaches were used to investigate the role of MMP\u201010 (matrix metalloproteinase 10) in vericiguat\u2010regulated VC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">Vericiguat treatment significantly reduced aortic calcification and osteogenic markers of VSMCs both in nephrectomy\u2010induced rats and adenine\u2010induced mice. It also inhibited calcium deposition and the phenotypic switch of VSMCs from a contractile to an osteoblastic state in both aortic ring and VSMC cultures. Transcriptomic profiling identified MMP\u201010 as a key mediator; MMP\u201010 was upregulated in VC models, and vericiguat reduced its expression. Overexpression of MMP\u201010 reversed the protective effects of vericiguat, and lentiviral\u2010mediated MMP\u201010 knockdown confirmed its procalcific role. Mechanistically, vericiguat increased cGMP\u2010PKG (cyclic guanosine monophosphate\u2010protein kinase G) signaling, including phosphorylated vasodilator\u2010stimulated phosphoprotein and phosphorylated c\u2010Jun (transcription factor Jun), ultimately downregulating MMP\u201010.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Vericiguat inhibits VSMC osteogenic differentiation and attenuates VC by modulating the cGMP\u2010PKG\u2010MMP\u201010 axis. These findings support vericiguat as a potential therapeutic candidate for VC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.046542","type":"journal-article","created":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T09:10:31Z","timestamp":1778058631000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Vericiguat Attenuates Vascular Calcification by Cyclic Guanosine Monophosphate\u2010Protein Kinase G Pathway Mediated Suppression of Matrix Metalloproteinase 10"],"prefix":"10.1161","volume":"15","author":[{"given":"Qing\u2010Yun","family":"Hao","sequence":"first","affiliation":[{"name":"Guangdong Provincial Clinical Research Center for Cancer","place":["Guangzhou, China"]},{"name":"The Affiliated Hospital of Inner Mongolia Medical University","place":["Hohhot, 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