Uqcr11, short for Ubiquinol-cytochrome c reductase, complex III subunit XI, is involved in oxidative phosphorylation, a key metabolic pathway in mitochondria responsible for ATP synthesis [1,3,4,5,6]. It is of great biological importance as it contributes to the proper functioning of the electron transport chain within the mitochondria, which is crucial for cellular energy production. Genetic models, such as KO/CKO mouse models, can be valuable for studying its functions.

In heart regeneration, Nat10 was found to repress Uqcr11 independently of its ac4C enzyme activity. This suppression weakens mitochondrial respiration and enhances glycolytic capacity in cardiomyocytes, leading to metabolic reprogramming. Overexpression of Nat10 in cardiomyocytes promotes cardiac regeneration and improves cardiac function after injury, while inhibiting Nat10 in neonatal mice cardiomyocytes inhibits heart regeneration [1]. In traumatic brain injury (TBI) mouse models, lower levels of Uqcr11 were observed in the cerebral cortex. Overexpression of Uqcr11 attenuated H2O2-or hypoxia-reoxygenation-induced damage in vitro and restored motor, learning, and memory in C57BL/6 mice after TBI by preventing oxidative stress and neuronal apoptosis [2].

In conclusion, Uqcr11 is essential for maintaining normal mitochondrial function through its role in oxidative phosphorylation. Studies using mouse models have revealed its significance in heart regeneration and response to TBI. Understanding Uqcr11 functions can potentially offer new therapeutic targets for these and other related disease conditions [1,2].