Emerging interactions between mitochondria and NAD+ metabolism in cardiometabolic diseases.

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.