Pank1, or pantothenate kinase 1, is a rate-limiting enzyme in CoA biosynthesis. CoA is an essential cofactor for intermediary metabolism, involved in processes like the tricarboxylic acid cycle, nutrient oxidation, histone acetylation, and synthesis of lipids, glycans, and haem [2].

In cardiac function studies, cardiomyocyte-specific Pank1 deletion (cmPank1-/-) in mice reduced PANK1 mRNA, protein, and CoA levels. When subjected to pressure overload, cmPank1-/-mice had more ventricular dilation and exacerbated cardiac fibrosis, with changes in fatty acid and ketone metabolism, suggesting Pank1's role in regulating fibrotic and metabolic processes during pressure overload [1]. In leptin-deficient mice, Pank1 deficiency reduced hyperglycaemia and hyperinsulinaemia, modified global metabolism, and improved aspects of the diabetic phenotype, although it did not affect insulin resistance [3].

In conclusion, Pank1 is crucial for CoA biosynthesis, which impacts various metabolic processes. Studies using Pank1 knockout mouse models have revealed its significance in cardiac function during pressure overload and in modifying the diabetic phenotype in leptin-deficient mice. These findings enhance our understanding of the role of Pank1 in disease-related metabolic and physiological processes.