Abstract
Insulin has an important regulatory effect on the heart, and the important regulatory effect of insulin on the heart is the regulation of substrate utilization. Studies have shown that aging is closely related to insulin resistance, and aging is thought to be one of the underlying causes of insulin resistance. Additionally, chronic inflammation is a major risk factor for aging and aging-related diseases. How to delay or reverse insulin resistance caused by aging is an important scientific problem. In the current study, we used cardiomyocyte cell lines and isolated heart cells as an in vitro model, and aged mice as in vivo model to study the effect of KAT7 on insulin resistance, and results showed that knockdown or inhibiting KAT7 can significantly increase the insulin sensitivity in vivo and in vitro. In addition, the knockdown of KAT7 could reduce inflammation and oxidative stress caused by aging. These findings indicate that KAT7 can be used as one of the potential targets for the treatment of insulin resistance caused by aging.