Lilly Underwood, Chun-sun Jiang, Joo-Yeun Oh, Priscila Y Sato
{"title":"Unheralded adrenergic receptor signaling in cellular oxidative stress and death","authors":"Lilly Underwood, Chun-sun Jiang, Joo-Yeun Oh, Priscila Y Sato","doi":"10.1016/j.cophys.2024.100766","DOIUrl":null,"url":null,"abstract":"<div><p>Catecholamines (CAs) bind and activate adrenergic receptors (ARs), thus exuding a key role in cardiac adaptations to global physiological queues. Prolonged exposure to high levels of CAs promotes deleterious effects on the cardiovascular system, leading to organ dysfunction and heart failure (HF). In addition to the prominent role of ARs in inotropic and chronotropic responses, recent studies have delved into elucidating mechanisms contributing to CA toxicity and cell death. Central to this process is understanding the involvement of α1AR and βAR in cardiac remodeling and mechanisms of cellular survival. Here, we highlight the complexity of AR signaling and the fundamental need for a better understanding of its contribution to oxidative stress and cell death. This crucial informational nexus remains a barrier to the development of new therapeutic strategies for cardiovascular diseases.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"40 ","pages":"Article 100766"},"PeriodicalIF":2.5000,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Opinion in Physiology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2468867324000324","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Catecholamines (CAs) bind and activate adrenergic receptors (ARs), thus exuding a key role in cardiac adaptations to global physiological queues. Prolonged exposure to high levels of CAs promotes deleterious effects on the cardiovascular system, leading to organ dysfunction and heart failure (HF). In addition to the prominent role of ARs in inotropic and chronotropic responses, recent studies have delved into elucidating mechanisms contributing to CA toxicity and cell death. Central to this process is understanding the involvement of α1AR and βAR in cardiac remodeling and mechanisms of cellular survival. Here, we highlight the complexity of AR signaling and the fundamental need for a better understanding of its contribution to oxidative stress and cell death. This crucial informational nexus remains a barrier to the development of new therapeutic strategies for cardiovascular diseases.
儿茶酚胺(CA)能结合并激活肾上腺素能受体(AR),因此在心脏适应全球生理变化的过程中发挥着关键作用。长期暴露于高水平的 CAs 会对心血管系统产生有害影响,导致器官功能障碍和心力衰竭(HF)。除了 ARs 在肌力和时脉反应中的突出作用外,最近的研究还深入探讨了导致 CA 毒性和细胞死亡的机制。这一过程的核心是了解α1AR和βAR参与心脏重塑和细胞存活的机制。在此,我们强调了 AR 信号传导的复杂性,以及更好地了解其对氧化应激和细胞死亡的贡献的根本必要性。这一重要的信息联系仍然是开发心血管疾病新疗法的障碍。