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.

中文翻译：

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心脏代谢疾病中线粒体和 NAD+ 代谢之间新出现的相互作用。


烟酰胺腺嘌呤二核苷酸 (NAD+) 是氧化还原反应必需的辅酶，可调节细胞分解代谢途径。 NAD+ 和线粒体之间存在着相互交织的关系，会对线粒体功能产生影响。 NAD+ 稳态失调会导致能量受损和氧化应激增加，从而导致心脏代谢疾病的发病机制。在这篇综述中，我们探讨了 NAD+ 稳态的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此类病理状况的并发症。此外，我们强调了线粒体 NAD+ 转运蛋白在调节细胞和线粒体 NAD+ 稳态中的潜在作用和治疗前景。