{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T21:40:17Z","timestamp":1773265217384,"version":"3.50.1"},"reference-count":65,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T00:00:00Z","timestamp":1773187200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Atherosclerosis, the cholesterol-driven inflammatory process underlying cardiovascular disease (CVD), remains the leading cause of death in high-income countries despite major advances in risk factor management. This underscores the urgent need for therapies that directly target plaque development and progression. Recent evidence has uncovered an important role for lymphatic vessels in cardiovascular health: by facilitating reverse cholesterol transport, lymphatics help clear excess cholesterol from arterial walls and influence atherosclerosis from its earliest stages to advanced disease. Enhancing lymphatic pumping before atherogenesis limits plaque formation, while restoring lymphatic function in established atherosclerosis reduces lesion size and promotes stabilization. CVD risk rises sharply after menopause, and lymphedema studies suggest that women experience a more pronounced age-related decline in lymphatic pumping than men, pointing to a potential link with hormonal fluctuations. Hormonal changes throughout life\u2014whether due to aging, therapeutic interventions, or personal choice\u2014are key determinants of CVD vulnerability. Yet, how these changes affect lymphatic transport in individuals predisposed to CVD remains unexplored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In this study, age-matched\n                      <jats:italic>\n                        Ldlr\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      males and ovariectomized females\u2014 in which estrogen levels were reduced to mimic the decline observed during menopause\u2014 were treated with 17\n                      <jats:italic>\u03b2<\/jats:italic>\n                      -estradiol (E2) to assess the impact of hormone therapy on\n                      <jats:italic>in vivo<\/jats:italic>\n                      lymphatic function and atherosclerosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In males, E2 reduced lesion burden and improved lymphatic transport without increasing the expression of key lymphatic endothelial and muscle cell genes involved in vessel integrity and function. In females, estrogen receptor\n                      <jats:italic>\u03b1<\/jats:italic>\n                      \u2014but not estrogen receptor\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2014was critical for lymphatic vessel function, and its downregulation reduced Flt4 mRNA abundance, a gene essential for lymphatic growth and pumping. E2 impaired lymphatic function in ovariectomized females; however, enhancing lymphatic transport beforehand prevented this effect and reduced atherosclerotic plaque formation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings reveal that estrogens modulate lymphatic function and atherosclerosis differently according to sex and baseline hormonal status. These results suggest that lymphatic function may contribute to the interplay between hormonal changes and cardiovascular risk, supporting the development of more targeted therapeutic strategies for populations undergoing hormonal transitions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2026.1699372","type":"journal-article","created":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T05:35:50Z","timestamp":1773207350000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Sex-specific lymphatic responses to estrogen shape atherosclerosis in high-risk mice"],"prefix":"10.3389","volume":"13","author":[{"given":"Mona","family":"Mesples","sequence":"first","affiliation":[{"name":"Department of Medicine, Faculty of Medicine, Universit\u00e9 de Montr\u00e9al","place":["Montreal, QC, Canada"]},{"name":"Montreal Heart Institute Research Center","place":["Montreal, QC, 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