ArticleFrontiers in cardiovascular medicine2026
Sex-specific lymphatic responses to estrogen shape atherosclerosis in high-risk mice.
Article in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: 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-whether due to aging, therapeutic interventions, or personal choice-are key determinants of CVD vulnerability. Yet, how these changes affect lymphatic transport in individuals predisposed to CVD remains unexplored. Methods: In this study, age-matched Results: 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 Conclusion: 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.
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