PDF(Pubmed)
Abstract：
Early life exposure lays the groundwork for the risk of developing cardiovascular-kidney-metabolic (CKM) syndrome in adulthood. Various environmental chemicals to which pregnant mothers are commonly exposed can disrupt fetal programming, leading to a wide range of CKM phenotypes. The aryl hydrocarbon receptor (AHR) has a key role as a ligand-activated transcription factor in sensing these environmental chemicals. Activating AHR through exposure to environmental chemicals has been documented for its adverse impacts on cardiovascular diseases, hypertension, diabetes, obesity, kidney disease, and non-alcoholic fatty liver disease, as evidenced by both epidemiological and animal studies. In this review, we compile current human evidence and findings from animal models that support the connection between antenatal chemical exposures and CKM programming, focusing particularly on AHR signaling. Additionally, we explore potential AHR modulators aimed at preventing CKM syndrome. As the pioneering review to present evidence advocating for the avoidance of toxic chemical exposure during pregnancy and deepening our understanding of AHR signaling, this has the potential to mitigate the global burden of CKM syndrome in the future.
摘要：
生命早期暴露为成年后发生心血管-肾脏-代谢综合征（CKM）的风险奠定了基础。孕妇经常接触的各种环境化学物质会破坏胎儿的编程，导致广泛的CKM表型。芳香烃受体（AHR）作为配体激活的转录因子在感知这些环境化学物质中具有关键作用。通过暴露于环境化学品激活AHR已被证明对心血管疾病产生不利影响。高血压,糖尿病,肥胖，肾病,和非酒精性脂肪性肝病,流行病学和动物研究都证明了这一点。在这次审查中,我们从动物模型中收集了当前的人类证据和发现，以支持产前化学暴露与CKM编程之间的联系，特别关注AHR信号。此外,我们探索旨在预防CKM综合征的潜在AHR调节剂.作为开创性的审查，提出的证据主张在怀孕期间避免有毒化学品暴露和加深我们对AHR信号的理解，这有可能减轻未来CKM综合征的全球负担.
