Uqcr11, short for Ubiquinol-cytochrome c reductase, complex III subunit XI, is involved in oxidative phosphorylation pathway, which is crucial for mitochondrial ATP synthesis coupled electron transport [3]. It plays an important role in maintaining normal mitochondrial function and overall cellular energy metabolism. Genetic models, such as KO/CKO mouse models, can be valuable tools to study its functions.

In heart regeneration, Nat10 represses Uqcr11 independently of its ac4C enzyme activity. This suppression leads to weakened mitochondrial respiration and enhanced glycolytic capacity in cardiomyocytes, promoting metabolic reprogramming and heart regeneration [1].

In traumatic brain injury, lower levels of Uqcr11 expression were found in the cerebral cortex of TBI mice. Overexpression of Uqcr11 attenuated H2O2-or hypoxia-reoxygenation-induced damage, prevented oxidative stress and neuronal apoptosis in vitro, and restored motor, learning, and memory in C57BL/6 mice after TBI [2].

In conclusion, Uqcr11 is essential for mitochondrial function and energy metabolism. Studies using mouse models have revealed its role in heart regeneration and response to traumatic brain injury. These findings contribute to understanding the underlying mechanisms of these biological processes and potential therapeutic targets for related diseases.