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. Author manuscript; available in PMC: 2022 Feb 17.
Published in final edited form as: Cell Rep. 2021 Nov 9;37(6):109971. doi: 10.1016/j.celrep.2021.109971

Figure 3. TMT-mass spectrometry (MS) of skeletal muscles undergoing atrophy induced by dexamethasone, LLC cancer cachexia, and aging reveals distinct proteomic signatures of stimulus-specific atrophy.

Figure 3.

(A–C) Volcano plots of TMT data and GSEA from TA muscles from (A) dexamethasone, (B) LLC cancer cachexia, and (C) aging.

(D) Comparison of significantly regulated proteins (p < 0.05 and log2FC > 0.3 for upregulated and log2FC < −0.3 for downregulated proteins) in distinct modes of myofiber atrophy. Relatively few of these up- and downregulated proteins showed overlap between dexamethasone, LLC cancer cachexia, and aging.

(E) Heatmap of the proteins which met the criteria above and shared overlap with at least 2 modes of atrophy.

(F) Atrogenes previously described as mediators of atrophy are not consistently regulated at the protein level.