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Transgenic mice expressing a cardiac dominant-negative (Dn) p38 antagonized cardiac I/R injury, and disruption of a single copy of p38 in mice was reported to be less susceptible to myocardial I/R injury [62, 63]

Specifically, the drug effectively inhibits the activation of the NF-B signaling pathway, leading to significant reduction in the mRNA expression levels of pro-inflammatory cytokines such as TNF-, IL-6, and IL-1, ultimately delaying the progression of muscle atrophy [29]

These analytical findings indicate that the models conclusions are robust to parameter uncertainty (Fig 2)