Skeletal muscle atrophy is a crippling disorder that develops as people age and get sick, but the underlying causes are still not fully understood. Previous research found that similar transcriptional alterations take place in muscle during atrophy brought on by various stressors. However, nothing is known about whether this is accurate at the proteome level. Contrary to this prior paradigm, we discover that diverse atrophic stressors (such as corticosteroids, cancer cachexia, and ageing) cause essentially unique mRNA and protein alterations during mouse muscle atrophy. Furthermore, the transcriptome-proteome gap is pervasive. As a result, atrophy markers (also known as atrogenes) discovered in prior microarray-based research does not show up in proteomics as typically produced by atrophy. As a result, atrophy markers (also known as atrogenes) discovered in prior microarray-based research does not show up in proteomics as typically produced by atrophy (Al Delaimy et al., 2002). Instead, we discover proteins (herein described as "atroproteins") that are specifically controlled by various forms of atrophy, such as the myokine CCN1/Cyr61, which controls myofiber type flipping during sarcopenia. These combined studies show that various catabolic stressors cause muscle atrophy through substantially separate pathways.
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