 This study found that a specific enzyme called phosphoblisterate mutase 5, PgAm5, plays a key role in mitochondrial function in diabetic cardiomyopathy. It was discovered that when PgAm5 is overexpressed in cardiomyocytes, it can reduce the amount of ATP produced, decrease respiration rates, and increase the time taken for mitochondria to open their pores. This suggests that PgAm5 may be responsible for the mitochondrial dysfunction seen in diabetic cardiomyopathy. Additionally, it was found that PgAm5 interacts with another protein called Prohibitin II, PhB2, which is involved in mitochondrial fusion and fission. When PgAm5 is dephosphorylated by PhB2, it leads to increased mitochondrial dysfunction. Finally, it was shown that mice with a genetic mutation that causes them to have more PgAm5 are protected against diabetic cardiomyopathy. This article was authored by Rong-Jun-Zou, Jun Tao, Jehi, and others. We are article.tv, links in the description below.