Moreover, numerous studies have demonstrated that oxidative stress can induce muscular atrophy via various mechanisms: (1) Upregulation of critical proteolytic proteins, including the muscle-specific E3 ligases such as ATROGIN-1; (2) release of cytosolic calcium ions, which activate Capn-1 and Casp3a; (3) oxidative conformational alterations in myofibrillar proteins, rendering them more vulnerable to degradation due to oxidation, resulting in their unfolding into the primary structure. The gene discussed is FBXO32; the disease is muscular atrophy.