The Role of Cell Death Modes Regulated by Copper Overload in Aging-related Atrophy for Skeletal Muscles
Skeletal muscle aging is a biological process that occurs as the body ages,characterized by mass loss and functional decline.The involvement of metallomics,particularly copper metallomics,is pivotal in understanding its functional roles.Copper metallomics manifests as copper overload with aging.It triggers toxic effects that activate apoptosis,pyroptosis,ferroptosis,cuproptosis and also promote α-sy-nuclein aggregation.The related signaling cascades can eventually promote metabolic turbulence and the loss of proteins,mitochondria,satellite cells and other cell contents in senescent myofibers,while cau-sing the degeneration and abnormality of neuromuscular junctions.This is a new physiopathgical mecha-nism of aging-related atrophy in skeletal muscles.Here we firstly review the molecular biological functions of copper in the regulatory networks of aging-related atrophy for skeletal muscles,the potential mecha-nisms of copper overload in senescent skeletal muscles,and the novel role of multiple signaling transduc-tion pathways associated with copper overload-induced cell death modes comprising apoptosis,pyroptosis,ferroptosis and cuproptosis in aging-related atrophy for skeletal muscles.We aim to provide potential mo-lecular targets and option choices for clinically applying copper chelation to improve and treat aging-relat-ed atrophy in skeletal muscles.
cell deathcopper metallomicsaging-related atrophy in skeletal musclecuproptosisα-synuclein(α-syn)
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