{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T22:14:20Z","timestamp":1792793660404,"version":"4.5.0"},"reference-count":90,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2024,9,10]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Pulmonary hypertension (PH) is a major complication linked to adverse outcomes in heart failure with preserved ejection fraction (HFpEF), yet no specific therapies exist for PH associated with HFpEF (PH-HFpEF). We have recently reported on the role of skeletal muscle SIRT3 (sirtuin-3) in modulation of PH-HFpEF, suggesting a novel endocrine signaling pathway for skeletal muscle modulation of pulmonary vascular remodeling.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              Using skeletal muscle-specific\n              <jats:italic toggle=\"yes\">Sirt3<\/jats:italic>\n              knockout mice (\n              <jats:italic toggle=\"yes\">Sirt3<\/jats:italic>\n              <jats:sup>skm-\/-<\/jats:sup>\n              ) and mass spectrometry-based comparative secretome analysis, we attempted to define the processes by which skeletal muscle SIRT3 defects affect pulmonary vascular health in PH-HFpEF.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              <jats:italic toggle=\"yes\">Sirt3<\/jats:italic>\n              <jats:sup>skm-\/-<\/jats:sup>\n              mice exhibited reduced pulmonary vascular density accompanied by pulmonary vascular proliferative remodeling and elevated pulmonary pressures. Comparative analysis of secretome by mass spectrometry revealed elevated secretion levels of LOXL2 (lysyl oxidase homolog 2) in SIRT3-deficient skeletal muscle cells. Elevated circulation and protein expression levels of LOXL2 were also observed in plasma and skeletal muscle of\n              <jats:italic toggle=\"yes\">Sirt3<\/jats:italic>\n              <jats:sup>skm-\/-<\/jats:sup>\n              mice, a rat model of PH-HFpEF, and humans with PH-HFpEF. In addition, expression levels of CNPY2 (canopy fibroblast growth factor signaling regulator 2), a known proliferative and angiogenic factor, were increased in pulmonary artery endothelial cells and pulmonary artery smooth muscle cells of\n              <jats:italic toggle=\"yes\">Sirt3<\/jats:italic>\n              <jats:sup>skm-\/-<\/jats:sup>\n              mice and animal models of PH-HFpEF. CNPY2 levels were also higher in pulmonary artery smooth muscle cells of subjects with obesity compared with nonobese subjects. Moreover, treatment with recombinant LOXL2 protein promoted pulmonary artery endothelial cell migration\/proliferation and pulmonary artery smooth muscle cell proliferation through regulation of CNPY2-p53 signaling. Last, skeletal muscle\u2013specific\n              <jats:italic toggle=\"yes\">Loxl2<\/jats:italic>\n              deletion decreased pulmonary artery endothelial cell and pulmonary artery smooth muscle cell expression of CNPY2 and improved pulmonary pressures in mice with high-fat diet\u2013induced PH-HFpEF.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>\n              This study demonstrates a systemic pathogenic impact of skeletal muscle SIRT3 deficiency in remote pulmonary vascular remodeling and PH-HFpEF. This study suggests a new endocrine signaling axis that links skeletal muscle health and SIRT3 deficiency to remote CNPY2 regulation in the pulmonary vasculature through myokine LOXL2. Our data also identify skeletal muscle SIRT3, myokine LOXL2, and CNPY2 as potential targets for the treatment of PH\n              <jats:italic toggle=\"yes\"\/>\n              -HFpEF.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.124.068624","type":"journal-article","created":{"date-parts":[[2024,5,28]],"date-time":"2024-05-28T09:00:42Z","timestamp":1716886842000},"page":"867-883","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":26,"title":["Skeletal Muscle SIRT3 Deficiency Contributes to Pulmonary Vascular Remodeling in Pulmonary Hypertension Due to Heart Failure With Preserved Ejection Fraction"],"prefix":"10.1161","volume":"150","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9210-8611","authenticated-orcid":true,"given":"Jia-Rong","family":"Jheng","sequence":"first","affiliation":[{"name":"Division of Pulmonary, Critical Care, Sleep and Occupational Medicine (J.-R.J., Y.B., T.C., A.F., 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(K.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8632-5791","authenticated-orcid":true,"given":"Joshua R.","family":"Huot","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology (J.R.H., R.F.M., Y.-C.L.), Indiana University School of Medicine, Indianapolis."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Todd","family":"Cook","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Sleep and Occupational Medicine (J.-R.J., Y.B., T.C., A.F., R.F.M., Y.-C.L.), Indiana University School of Medicine, Indianapolis."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda","family":"Fisher","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Sleep and Occupational Medicine (J.-R.J., Y.B., T.C., A.F., R.F.M., Y.-C.L.), Indiana University School of Medicine, 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