Core Insights - The article discusses the development of organoid models for studying human vascular aging and neural tube development, highlighting the molecular mechanisms involved in these processes [2][4][8]. Vascular Organoid Model - The vascular organoid model simulates Hutchinson-Gilford Progeria Syndrome (HGPS), revealing that downregulation of the SRF pathway drives vascular aging [4][7]. - The model reproduces various pathological features of HGPS, including accelerated aging protein accumulation and impaired vascular barrier function [7]. - SRF is identified as a key regulatory factor in vascular aging, with its expression significantly downregulated in both HGPS models and naturally aging non-human primate tissues [7]. - Functional experiments show that knocking down SRF replicates vascular aging phenotypes, while overexpressing SRF improves cell morphology and restores angiogenic capacity [7]. Neural Organoid Model - The neural organoid model reveals the critical role of YAP as a mechanosensor in neural tube morphogenesis [8][12]. - YAP deficiency disrupts the apical-basal polarity of neural stem/progenitor cells, leading to structural abnormalities in neural rosettes [12]. - The study identifies a regulatory axis involving YAP, TEAD4, and LEF1, which is essential for neural tube development, demonstrating the interplay between mechanical and biochemical signals [12]. Future Implications - The findings from both vascular and neural organoid models provide new insights into the molecular mechanisms of organ homeostasis, aging, and development [14][15]. - These results may pave the way for early diagnosis and targeted therapeutic strategies for related diseases [15].