MTCH2, a member of the solute carrier 25 family, is located on the outer mitochondrial membrane [2]. It functions as a mitochondrial outer membrane protein insertase, being required for the insertion of diverse transmembrane proteins [1]. MTCH2 is also involved in multiple biological pathways, such as mitochondrial apoptosis, fusion/fission, metabolic shift, and epithelial-mesenchymal transition, and thus is of great biological importance in processes like embryonic development, reproduction, and in various disease states [2]. Genetic models, especially knockout models, are valuable for studying its functions.

In Drosophila, knockdown of Mtch in heart tubes led to a dilated and poorly functioning heart tube, reduced adiposity, and shortened lifespan, along with impaired oxygen consumption in the presence of glucose [4]. In mice, adipose-specific MTCH2 depletion protected against high-fat-diet-induced obesity and metabolic disorders by stimulating thermogenesis in brown adipose tissue and browning of subcutaneous white adipose tissue [3]. These loss-of-function experiments reveal MTCH2's role in metabolism-related disease conditions.

In conclusion, MTCH2 is crucial for mitochondrial protein insertion and for regulating mitochondrial functions in various biological processes. Gene knockout models, such as in Drosophila and mice, have been instrumental in uncovering its role in metabolic diseases, neurodegenerative diseases, cancers, embryonic development, and reproduction [2,3,4]. This research on MTCH2 provides insights into disease mechanisms and potential therapeutic targets.