{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T11:48:05Z","timestamp":1789732085090,"version":"4.0.1"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2025,5,16]],"date-time":"2025-05-16T00:00:00Z","timestamp":1747353600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82030006"],"award-info":[{"award-number":["82030006"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82070435"],"award-info":[{"award-number":["82070435"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82370426"],"award-info":[{"award-number":["82370426"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82070245"],"award-info":[{"award-number":["82070245"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270250"],"award-info":[{"award-number":["82270250"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National key research and development","award":["2022YFA1104200"],"award-info":[{"award-number":["2022YFA1104200"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,7,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Thoracic aortic dissection (TAD) is a highly fatal disease lacking effective pharmacologic interventions in clinical practice. Emerging evidence indicates that the natriuretic peptide receptor C (NPR-C) plays a crucial role in the regulation of cardiovascular diseases. However, the precise involvement of NPR-C in TAD remains elusive. In this study, the role and molecular mechanisms of NPR-C in the pathogenesis of TAD were investigated.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Through integrated analyses of human TAD transcriptome and single-cell sequencing data sets, we identified that NPR-C was downregulated in the aortas of acute TAD patients and in beta-aminopropionitrile (BAPN)-treated mice. Intriguingly, vascular smooth muscle cell (VSMC)-specific NPR-C knockout (NPR-CSMKO) mice, rather than endothelial cell-specific NPR-C knockout mice, developed TAD after treated with angiotensin II (Ang II) plus high salt diet (HSD), but not Ang II alone. Loss of NPR-C function promoted extracellular matrix degeneration, VSMCs apoptosis, and inflammation. RNA-sequencing analysis revealed that mitochondrial fatty acid oxidation (FAO) genes were significantly downregulated in the thoracic aortas of NPR-CSMKO mice treated with Ang II plus HSD. Notably, the expression of HADHB, a subunit of mitochondrial trifunctional protein (MTP) responsible for FAO, was obviously decreased in NPR-CSMKO mice treated with Ang II plus HSD. Mechanistically, knockdown of NPR-C activated ERK1\/2 pathway, which decreased the expression and activity of peroxisome proliferator-activated receptor \u03b3 (PPAR\u03b3) and inhibited HADHB expression. Furthermore, NPR-C agonist, C-ANP4\u201323, mitigated the progression of TAD in BAPN-treated mice. Activation of MTP by spermidine (SPD) effectively prevented TAD formation in NPR-CSMKO mice treated with Ang II plus HSD.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Our data highlight a critical role of HSD in triggering TAD and a previously unrecognized role of NPR-C that protects against TAD through regulating mitochondrial homeostasis. Therefore, NPR-C activation and SPD supplementation could be new prevention and treatment strategies for TAD.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvaf085","type":"journal-article","created":{"date-parts":[[2025,5,16]],"date-time":"2025-05-16T10:21:10Z","timestamp":1747390870000},"page":"1121-1134","source":"Crossref","is-referenced-by-count":4,"title":["Deficiency of NPR-C triggers high salt-induced thoracic aortic dissection by impairing mitochondrial homeostasis"],"prefix":"10.1093","volume":"121","author":[{"given":"Jin-Qiu","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine, Department of Hypertension, Ruijin Hospital and State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine , Ruijin 2nd Road 197, Shanghai 200025 ,","place":["China"]},{"name":"Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Shandong First Medical University , 16766 Jinshi Road, Jinan 250014 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8913-0220","authenticated-orcid":false,"given":"Yi","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine , Ruijin 2nd Road 197, Shanghai 200025 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen-Hui","family":"Zhai","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Department of Hypertension, Ruijin Hospital and State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiao Tong 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