Micu1, short for mitochondrial calcium uptake 1, is a key molecule in mitochondrial calcium regulation. It plays a vital role in maintaining the normal function, survival, and death of endothelial cells. Mitochondrial calcium homeostasis, in which Micu1 is involved, is crucial for various cellular processes. Genetic models, such as KO/CKO mouse models, have been valuable in studying its function [1,2].

In endothelial-specific Micu1ecKO (conditional knockout) mice, Micu1 deficiency led to exacerbated cardiac hypertrophy, interstitial myocardial fibrosis, and further reduction in left ventricular function in diabetic mice, suggesting its protective role in diabetic cardiomyopathy (DCM) [1]. In murine genetic models, MICU1 deletion altered cardiomyocyte mitochondrial calcium signaling and energy metabolism, highlighting its role in cardiac mitochondrial Ca2+ influx [2]. MICU1 knockout mice also displayed disorganized mitochondrial architecture, and MICU1 ablation resulted in altered cristae organization, mitochondrial ultrastructure, mitochondrial membrane dynamics, and cell death signaling [3].

In conclusion, Micu1 is essential for regulating mitochondrial calcium homeostasis, mitochondrial architecture, and cristae structure. Its deficiency is associated with detrimental effects in diseases like diabetic cardiomyopathy and disruptions in cardiac function. Studies using Micu1 KO/CKO mouse models have provided crucial insights into its role in these disease conditions, helping to understand the underlying mechanisms and potentially identify new therapeutic targets [1,2,3].