MTCH2, short for mitochondrial carrier homolog 2, is a member of the solute carrier 25 family located on the outer mitochondrial membrane. It functions as a mitochondrial outer membrane protein insertase, required for inserting various types of proteins [1]. MTCH2 is also involved in multiple biological processes like mitochondrial apoptosis, fusion/fission, metabolic shift, and epithelial-mesenchymal transition, thus having a crucial impact on metabolic diseases, neurodegenerative diseases, cancers, embryonic development, and reproduction [2].

In Drosophila, knocking down Mtch in heart tubes led to a dilated and poorly functioning heart tube, reduced adiposity, and shortened lifespan. Cardiac Mtch mutants had impaired oxygen consumption in the presence of glucose. This indicates that MTCH2 reduction may be beneficial when fatty acids are the major fuel source but maladaptive in heart failure where glucose is more utilized [4]. In mice, adipose-specific MTCH2 depletion protected against high-fat-diet-induced obesity and metabolic disorders by promoting energy expenditure through stimulating thermogenesis and browning of adipose tissue [3].

In summary, MTCH2 plays essential roles in mitochondrial function-related biological processes. Studies using gene-knockout models in flies and mice have revealed its significance in heart function, obesity, and metabolic diseases, providing insights into potential therapeutic targets for these conditions.