Car3, short for Carbonic Anhydrase 3, is an enzyme belonging to the carbonic anhydrase family. It catalyzes the reversible condensation of water and carbon dioxide to carbonic acid, which then dissociates to bicarbonate. This function is crucial in multiple biological processes, with its activity potentially influencing various physiological functions related to acid-base balance and metabolism [2].

In a study on myocardial infarction (MI), Car3 deficiency in mice led to weakened collagen density, enlarged infarct size, and aggravated cardiac dysfunction post-MI. CAR3 up-regulation was observed in cardiac fibroblasts in the infarct area during the reparative phase of MI. Mechanistically, CAR3 stabilizes Smad7 protein by modulating its acetylation, dampening phosphorylation of Smad2 and Smad3, and thus promoting fibroblast activation via the Smad7-TGF-β/Smad2/3 signaling pathway, which is essential for cardiac repair post-MI [1].

In another study, knockout of Car3 in mice did not show significant differences in de novo lipogenesis or responses to high-fat diet compared to wild-type mice, indicating that Car3 is not required for fatty acid synthesis and does not protect against high-fat diet-induced obesity [2]. Also, in an experimental autoimmune myasthenia gravis animal model, inhibition of CAR3 promoted CHRN internalization in skeletal muscle cells, leading to accelerated degradation of postsynaptic CHRN, suggesting a role for CAR3 in maintaining CHRN homeostasis at the neuromuscular junction [3].

In conclusion, Car3 plays important roles in cardiac repair post-MI, maintaining neuromuscular junction homeostasis, and is not essential for fatty acid synthesis or protection against high-fat diet-induced obesity. Gene knockout mouse models have been valuable in revealing these functions of Car3, providing insights into its role in specific disease conditions such as myocardial infarction and myasthenia gravis.