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. 2023 Mar 3;10:1099143. doi: 10.3389/fnut.2023.1099143

Figure 3.

Figure 3

The inflammatory factor tumor necrosis factor-alpha (TNF-α) can induce the apoptosis of skeletal muscle cells and lead to the accumulation of reactive oxygen species (ROS). The collection of ROS can lead to mitochondrial dysfunction and depolarization, while TNF-α can activate the MAPK signaling pathway and cause nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). NF-κB expression levels to increase, inducing inflammation and protein degradation. Tumor necrosis factor-related weak apoptosis-inducing factor (TWEAK) can activate NF-κB signaling to promote proteolysis and simultaneously increase the expression level of fibroblast growth factor-inducing factor 14 (Fn14), both of which act synergistically in the process of skeletal muscle atrophy. IL-1 (Interleukin 1) and IL-6 (Interleukin 6) are critical inflammatory factors that induce skeletal muscle atrophy. IL-1 stimulates the expression of IL-6 by stimulating the expression of NF-κB. Overexpression of IL-1 and IL-6 induces an inflammatory response in the body and thus induces skeletal muscle atrophy.