Hormonal
Chronic systemic inflammation drives skeletal muscle atrophy by directly activating pro-catabolic signaling pathways (NF-κB, JAK/STAT, p38MAPK) that increase protein degradation via UPS/ALP and inhibit protein synthesis via IGF-1/Akt/mTOR suppression.
If you are experiencing muscle loss alongside a chronic inflammatory condition (like autoimmune disease, diabetes, or chronic infection), standard resistance training and high protein intake may be insufficient on their own. Medical management of the underlying inflammation is critical to stop the biological signals that actively break down muscle tissue.
Inflammation directly influences skeletal muscle through the activation of receptor-mediated intramuscular signaling pathways, including the NF-κB, JAK/STAT, and p38MAPK pathways... These target genes act on UPS, causing proteolysis and triggering skeletal muscle atrophy.
Why this rating
This is a review paper summarizing extensive in vivo and in vitro evidence; while not a single clinical trial, the mechanistic consensus is strong.
Source
Inflammation: Roles in Skeletal Muscle Atrophy
Yanan Ji et al. · Antioxidants · 2022
DOI 10.3390/antiox11091686
More from this paper
- Inflammation indirectly causes muscle atrophy by dysregulating the Hypothalamic-Pituitary-Adrenal (HPA) axis, leading to excessive glucocorticoid release, which further inhibits muscle protein synthesis and promotes proteolysis.Good
- Myostatin (MSTN) levels are increased by inflammatory factors (TNF-α, IL-6) and act as a negative regulator of muscle mass by activating the Smad2/3 pathway, which upregulates E3 ubiquitin ligases (MuRF1, Atrogin-1) and inhibits satellite cell recruitment.Good
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