Samm50, the sorting and assembly machinery component, is a mitochondrial outer membrane protein. It is involved in protein sorting and assembly, and plays a key role in mitochondrial dynamics and quality control through regulating mitophagy. It also participates in pathways related to maintaining cellular homeostasis, such as piecemeal basal - and OXPHOS - induced mitophagy [2,6].

Samm50 has been studied in various disease - related contexts. In neonatal cardiomyocytes, knockdown and overexpression experiments via lentiviruses showed that Samm50 promotes hypertrophy by regulating Pink1 - dependent mitophagy signaling. Its deficiency - mediated protection against cardiac hypertrophy is abolished by inhibiting mitophagy [1]. In beige adipocytes differentiated from human adipose - derived stem cells, knockdown and overexpression of Samm50 affected the balance between mitochondrial fusion and fission, thereby regulating thermogenesis [4]. In non - alcoholic fatty liver disease (NAFLD), certain single nucleotide polymorphisms of Samm50 are associated with an increased risk of the disease. In vitro studies indicated that Samm50 deficiency leads to increased lipid accumulation due to decreased fatty acid oxidation [3,7]. In addition, in hypoxia - induced cardiac injury, overexpression and knockdown of Samm50 mitigated and exacerbated cardiac apoptosis and fibrosis respectively, with Shmt2 interacting with Samm50 being a key regulator in this process [5].

In conclusion, Samm50 is essential for mitochondrial - related functions like mitophagy, mitochondrial dynamics, and thermogenesis. Its dysregulation is associated with diseases such as cardiac hypertrophy, NAFLD, and hypoxia - induced cardiac injury. Studies using knockdown and overexpression models have been crucial in uncovering its role in these biological processes and disease conditions, providing potential insights for therapeutic strategies.