Mfn1, short for Mitofusin 1, is a key protein in regulating mitochondrial fusion. Mitochondrial fusion is crucial for maintaining normal mitochondrial function and is involved in various cellular activities such as energy production, metabolism, and cell survival. Mfn1 forms homotypic and heterotypic complexes with Mfn2, and these complexes play a vital role in promoting mitochondrial fusion [1].

Mice deficient in Mfn1 die in mid-gestation, highlighting its essential role in embryonic development [1]. In denervation-induced skeletal muscle atrophy, miR-142a-5p targets Mfn1, disrupting the tubular mitochondrial network and leading to mitochondrial dysfunction, mitophagy, and apoptosis [2]. Also, in environmental cadmium-induced testicular testosterone decline, Parkin-dependent Mfn1 degradation causes mitochondrial fusion disorder, suppressing T synthesis in Leydig cells [3].

In conclusion, Mfn1 is essential for mitochondrial fusion and thus for many biological processes. Gene-knockout mouse models have revealed its crucial roles in embryonic development, skeletal muscle atrophy, and testicular testosterone synthesis, providing valuable insights into related disease mechanisms.