<p>As life expectancy increases, age-related diseases are becoming more prevalent. While these conditions are traditionally studied in isolation, mounting evidence points to shared, systemic mechanisms underlying these conditions. Our research highlights the vasculature as a key player in organ homeostasis and repair, and a system shared across all organs—making its dysfunction potential driver of age-related pathologies.</p><p>We demonstrate that manipulating <strong>VEGF signaling</strong> to counteract age-related microvascular rarefaction promotes <strong>comprehensive geroprotection</strong>, preserving organ function and delaying disease onset. Our findings also reveal a link between vascular rarefaction and altered RNA splicing. While hypoxia-driven and age-related changes in alternative RNA splicing have been studied independently, we propose a unifying mechanism that links the two. To explore this further, we also employ patient-derived organoids, which retain their biological age in culture, providing a robust in vitro platform to test anti-aging interventions.</p><p>Our findings support a <strong>vascular theory of aging</strong>, identifying vascular health as a promising target to mitigate age-related diseases and promote healthier aging.</p>
