{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:34:40Z","timestamp":1791995680330,"version":"4.4.0"},"reference-count":532,"publisher":"SAGE Publications","issue":"12","license":[{"start":{"date-parts":[[2021,10,1]],"date-time":"2021-10-01T00:00:00Z","timestamp":1633046400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2021,10]]},"abstract":"<jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>The vasculature responds to the respiratory needs of tissue by modulating luminal diameter through smooth muscle constriction or relaxation. Coronary perfusion, diastolic function, and coronary flow reserve are drastically reduced with aging. This loss of blood flow contributes to and exacerbates pathological processes such as angina pectoris, atherosclerosis, and coronary artery and microvascular disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Advances:<\/jats:title>\n                    <jats:p>Increased attention has recently been given to defining mechanisms behind aging-mediated loss of vascular function and development of therapeutic strategies to restore youthful vascular responsiveness. The ultimate goal aims at providing new avenues for symptom management, reversal of tissue damage, and preventing or delaying of aging-induced vascular damage and dysfunction in the first place.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Critical Issues:<\/jats:title>\n                    <jats:p>\n                      Our major objective is to describe how aging-associated mitochondrial dysfunction contributes to endothelial and smooth muscle dysfunction\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      dysregulated reactive oxygen species production, the clinical impact of this phenomenon, and to discuss emerging therapeutic strategies. Pathological changes in regulation of mitochondrial oxidative and nitrosative balance (Section 1) and mitochondrial dynamics of fission\/fusion (Section 2) have widespread effects on the mechanisms underlying the ability of the vasculature to relax, leading to hyperconstriction with aging. We will focus on flow-mediated dilation, endothelial hyperpolarizing factors (Sections 3 and 4), and adrenergic receptors (Section 5), as outlined in\n                      <jats:xref ref-type=\"fig\">Figure 1<\/jats:xref>\n                      . The clinical implications of these changes on major adverse cardiac events and mortality are described (Section 6).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Future Directions:<\/jats:title>\n                    <jats:p>\n                      We discuss antioxidative therapeutic strategies currently in development to restore mitochondrial redox homeostasis and subsequently vascular function and evaluate their potential clinical impact (Section 7).\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      35, 974\u20131015.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2021.0031","type":"journal-article","created":{"date-parts":[[2021,7,27]],"date-time":"2021-07-27T13:04:46Z","timestamp":1627391086000},"page":"974-1015","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":36,"title":["Aging-Induced Impairment of Vascular Function: Mitochondrial Redox Contributions and Physiological\/Clinical Implications"],"prefix":"10.1177","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6689-0216","authenticated-orcid":false,"given":"Evan Paul","family":"Tracy","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Louisville, Louisville, Kentucky, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Hughes","sequence":"additional","affiliation":[{"name":"Department of Medicine and Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason E.","family":"Beare","sequence":"additional","affiliation":[{"name":"Cardiovascular Innovation Institute, University of Louisville, Louisville, Kentucky, USA."},{"name":"Kentucky Spinal Cord Injury Research Center, University of Louisville, Louisville, Kentucky, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabrielle","family":"Rowe","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Louisville, Louisville, Kentucky, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Beyer","sequence":"additional","affiliation":[{"name":"Department of Medicine and Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda Jo","family":"LeBlanc","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Louisville, Louisville, Kentucky, USA."},{"name":"Cardiovascular Innovation Institute, University of Louisville, Louisville, Kentucky, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2021,10,4]]},"reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mad.2016.02.007"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000105680.92873.70"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.109.213116"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.3.1185"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.exger.2015.01.044"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-43761-y"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00472.2017"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2020.12.021"},{"key":"e_1_3_4_10_2","doi-asserted-by":"publisher","DOI":"10.1155\/2019\/7169275"},{"key":"e_1_3_4_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.05.014"},{"key":"e_1_3_4_12_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2010.202838"},{"key":"e_1_3_4_13_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10541-005-0102-7"},{"key":"e_1_3_4_14_2","doi-asserted-by":"publisher","DOI":"10.1080\/10715760701481461"},{"key":"e_1_3_4_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2008.03.020"},{"key":"e_1_3_4_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.scr.2013.01.002"},{"key":"e_1_3_4_17_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.9.960"},{"key":"e_1_3_4_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.nutres.2020.03.002"},{"key":"e_1_3_4_19_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.116.310316"},{"key":"e_1_3_4_20_2","doi-asserted-by":"publisher","DOI":"10.1136\/hrt.2008.150888"},{"key":"e_1_3_4_21_2","first-page":"H1283","article-title":"Hydrogen peroxide relaxes porcine coronary arteries by stimulating BKCa channel activity","volume":"275","author":"Barlow RS","year":"1998","unstructured":"Barlow RS, and White RE. 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