线粒体与NAD代谢在心脏代谢疾病中的新出现的相互作用。
Emerging interactions between mitochondria and NAD metabolism in cardiometabolic diseases.
作者信息
Nasuhidehnavi Azadeh, Zarzycka Weronika, Górecki Ignacy, Chiao Ying Ann, Lee Chi Fung
机构信息
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA; Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, Binghamton University, Binghamton, NY 13790, USA.
Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA; Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
出版信息
Trends Endocrinol Metab. 2025 Feb;36(2):176-190. doi: 10.1016/j.tem.2024.07.010. Epub 2024 Aug 27.
Nicotinamide adenine dinucleotide (NAD) is an essential coenzyme for redox reactions and regulates cellular catabolic pathways. An intertwined relationship exists between NAD and mitochondria, with consequences for mitochondrial function. Dysregulation in NAD homeostasis can lead to impaired energetics and increased oxidative stress, contributing to the pathogenesis of cardiometabolic diseases. In this review, we explore how disruptions in NAD homeostasis impact mitochondrial function in various cardiometabolic diseases. We discuss emerging studies demonstrating that enhancing NAD synthesis or inhibiting its consumption can ameliorate complications of this family of pathological conditions. Additionally, we highlight the potential role and therapeutic promise of mitochondrial NAD transporters in regulating cellular and mitochondrial NAD homeostasis.
烟酰胺腺嘌呤二核苷酸（NAD）是氧化还原反应的必需辅酶，可调节细胞分解代谢途径。NAD与线粒体之间存在着相互交织的关系，对线粒体功能产生影响。NAD稳态失调可导致能量代谢受损和氧化应激增加，从而促进心脏代谢疾病的发病机制。在这篇综述中，我们探讨了NAD稳态破坏如何影响各种心脏代谢疾病中的线粒体功能。我们讨论了新出现的研究，这些研究表明增强NAD合成或抑制其消耗可以改善这类病理状况的并发症。此外，我们强调了线粒体NAD转运体在调节细胞和线粒体NAD稳态中的潜在作用和治疗前景。
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