{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T06:55:49Z","timestamp":1791528949286,"version":"4.3.4"},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,8,2]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Emerging evidence indicates that impaired angiogenesis may contribute to hypertension\u2010induced cardiac remodeling. The nicotinamide adenine dinucleotide\u2013dependent deacetylase Sirtuin 3 (\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3) has the potential to modulate angiogenesis, but this has not been confirmed. As such, the aim of this study was to examine the relationship between\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3\u2010mediated angiogenesis and cardiac remodeling.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Our experiments were performed on\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3 knockout and age\u2010matched wild\u2010type mice infused with angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              (1400\u00a0ng\/kg per minute) or saline for 14\u00a0days. After angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              infusion,\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3 knockout mice developed more severe microvascular rarefaction and functional hypoxia in cardiac tissues compared with wild\u2010type mice. These events were concomitant with mitochondrial dysfunction and enhanced collagen I and collagen\n              <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>\n              expression, leading to cardiac fibrosis. Silencing\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3 facilitated angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              \u2013induced aberrant Pink\/Parkin acetylation and impaired mitophagy, while excessive mitochondrial reactive oxygen species generation limited angiogenic capacity in primary mouse cardiac microvascular endothelial cells. Moreover,\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3 overexpression in cardiac microvascular endothelial cells enhanced Pink\/Parkin\u2010mediated mitophagy, attenuated mitochondrial reactive oxygen species generation, and restored vessel sprouting and tube formation. In parallel, endothelial cell\u2013specific\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3 transgenic mice showed decreased fibrosis, as well as improved cardiac function and microvascular network, compared with wild\u2010type mice with similar stimuli.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Collectively, these findings suggest that\n              <jats:styled-content style=\"fixed-case\">SIRT<\/jats:styled-content>\n              3 could promote angiogenesis through attenuating mitochondrial dysfunction caused by defective mitophagy.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.117.006114","type":"journal-article","created":{"date-parts":[[2017,9,1]],"date-time":"2017-09-01T18:25:38Z","timestamp":1504290338000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":123,"title":["Sirtuin 3 Deficiency Accelerates Hypertensive Cardiac Remodeling by Impairing Angiogenesis"],"prefix":"10.1161","volume":"6","author":[{"given":"Tong","family":"Wei","sequence":"first","affiliation":[{"name":"State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gaojian","family":"Huang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Gao","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenglin","family":"Huang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengwei","family":"Sun","sequence":"additional","affiliation":[{"name":"Key Laboratory of State General Administration of Sport, Shanghai Research Institute of Sports Science, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Wu","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan","family":"Bu","sequence":"additional","affiliation":[{"name":"Department of Macromolecular Science, State Key Laboratory of Molecular Engineering of Polymers, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weili","family":"Shen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000256279.49882.d8"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.02149"},{"key":"e_1_3_5_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.114.300507"},{"key":"e_1_3_5_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/jhh.2009.63"},{"key":"e_1_3_5_6_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI24682"},{"key":"e_1_3_5_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10059-013-0130-x"},{"key":"e_1_3_5_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.01636-07"},{"key":"e_1_3_5_9_2","first-page":"2758","article-title":"SIRT3 blocks the cardiac hypertrophic response by augmenting Foxo3a\u2010dependent antioxidant defense mechanisms in mice","volume":"119","author":"Sundaresan NR","year":"2009","unstructured":"Sundaresan NR, Gupta M, Kim G, Rajamohan SB, Isbatan A, Gupta MP. 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