Sanford-Burnham Medical Research Institute, Development and Aging Program, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Cell. 2011 Dec 9;147(6):1422-1422.e1. doi: 10.1016/j.cell.2011.11.034.
Retinoic acid (RA), a lipid soluble signaling molecule derived from vitamin A (retinol), regulates diverse biological processes, including cellular proliferation, differentiation, and apoptosis, throughout embryonic development. RA controls the expression of genes involved in patterning and morphogenesis during organogenesis. Disruptions in the regulation of RA signaling results in several developmental disorders, including limb and skeletal defects, abnormal patterning of the central nervous system, ocular and craniofacial defects, cardiac malformation, foregut endoderm defects, and renal agenesis. Identification of pleiotropic functions for RA during organogenesis has provided a better understanding of cellular and molecular events controlling embryonic development. Loss-of-function studies using mutants of RA-synthesizing enzymes and RA receptors (RARs) have been particularly helpful in unraveling the mechanism of RA signaling. Further studies using genetic models are required to fully understand the molecular logic of RA signaling from embryogenesis to adulthood.
视黄酸（RA）是一种脂溶性信号分子，来源于维生素 A（视黄醇），在胚胎发育过程中调节多种生物学过程，包括细胞增殖、分化和凋亡。RA 控制器官发生过程中涉及形态发生和模式形成的基因表达。RA 信号转导的调节紊乱会导致多种发育障碍，包括肢体和骨骼缺陷、中枢神经系统异常模式形成、眼和颅面缺陷、心脏畸形、前肠内胚层缺陷和肾发育不全。在器官发生过程中对 RA 多效性功能的鉴定为控制胚胎发育的细胞和分子事件提供了更好的理解。使用 RA 合成酶和 RA 受体（RAR）突变体的功能丧失研究对于揭示 RA 信号转导机制特别有帮助。需要使用遗传模型进一步研究，以充分了解从胚胎发生到成年期的 RA 信号的分子逻辑。
