Plin5, also known as perilipin 5, is a protein that coats lipid droplets (LDs) and is significantly involved in lipid metabolism [1]. It plays a crucial role in regulating the key metabolic processes of intracellular lipid accumulation, which is associated with several metabolic diseases [1]. Plin5 is also related to reactive oxygen species (ROS) production originated from mitochondria in the heart, and is thus involved in the development of diabetic cardiomyopathy [1].

In Plin5 -/- mice, isolated cardiomyocytes store less LDs, but have a transient increase in intracellular fatty acid oxidation intermediates and show improved tolerance to hypoxia [2]. In T2DM-HFFA mice, Plin5 deficiency reduces the number of cardiac capillaries, worsens structural incompleteness, and enhances diastolic dysfunction [3]. In a vascular injury model, Plin5 knockdown in C57BL/6J mice leads to accelerated neointima hyperplasia, excessive proliferation, and migration of vascular smooth muscle cells (VSMCs) [4].

In conclusion, Plin5 is vital for maintaining lipid metabolism balance and normal physiological functions. Its deficiency in mouse models reveals its importance in diseases such as diabetic cardiomyopathy, cardiac microvascular impairment, and vascular neointima hyperplasia. Research on Plin5 provides insights into understanding the mechanisms of these diseases and may help develop new therapeutic strategies.