Rcan1, short for Regulator of calcineurin 1, is a crucial gene with its primary function being the inhibition of the phosphatase calcineurin, and it also regulates mitochondrial function [4]. It is involved in pathways such as the calcineurin/NFAT transcriptional pathway, and plays a significant role in various biological processes including synaptic plasticity, development and maintenance of the cardiovascular system, and is associated with multiple diseases [4,5]. Genetic models like KO/CKO mouse models are valuable for studying Rcan1.

In cardiovascular diseases, RCAN1 reduction protects against atherosclerosis by reducing the uptake of oxidized low-density lipoproteins, while RCAN1 has a protective effect on myocardial ischemia/reperfusion injury, myocardial hypertrophy and intramural hematoma/aortic rupture [1]. In septic cardiomyopathy, RCAN1 -/- mice showed severe cardiac function impairment, increased myocardial hypertrophy and fibrosis, and aggravated mitochondrial injury, indicating that RCAN1 deficiency worsens the condition [3]. In diabetic cardiomyopathy, knockdown of RCAN1 improved cardiac dysfunction, lipid accumulation, and mitochondrial fission in db/db mice [2].

In conclusion, Rcan1 is essential in regulating mitochondrial function and calcineurin activity. Studies using KO/CKO mouse models have revealed its roles in cardiovascular diseases, septic cardiomyopathy, and diabetic cardiomyopathy. Understanding Rcan1 through these models provides insights into the mechanisms of these diseases and potential therapeutic strategies.