Nicotinamide Riboside: A Promising Treatment for Type 1 Cardiorenal Syndrome in Myocardial Infarction-Induced Acute Kidney Injury by Upregulating Nicotinamide Phosphoribosyltransferase-Mediated Nicotinamide Dinucleotide Levels.

ABSTRACT:

Background

Cardiorenal syndrome type 1 is characterized by the development of acute kidney injury following acute cardiac illness and notably acute myocardial infarction (MI). Acute kidney injury is considered an independent risk factor that increases mortality rate substantially. Nicotinamide adenine dinucleotide (NAD) is an important coenzyme in energy metabolism and oxidative phosphorylation, and in its oxidized form it is a substrate for multiple NAD⁺-dependent enzymes such as sirtuins and poly-ADP ribose polymerases. Decreased cardiac NAD levels, along with a downregulation of NAMPT (nicotinamide phosphoribosyl transferase), have been reported following MI. A compensatory upregulation in NMRK (nicotinamide riboside kinase) 2, an NAD⁺ biosynthetic enzyme t

SUBMITTER: Habeichi NJ 

PROVIDER: S-EPMC12132627 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature