Research
Hormonal
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.
High levels of inflammatory cytokines can increase Myostatin, a protein that naturally limits muscle growth. In chronic disease, this system is overactive, contributing to muscle loss. Therapies targeting Myostatin or its receptors are being investigated to counteract this loss.
GoodSupportsHIGH confidence
Factors such as chronic or acute inflammation, oxidative stress, angiotensin II, and glucocorticoids may all increase MSTN synthesis... Excessive MSTN can over-activate the MSTN-Smad2/3 pathway, which subsequently promotes proteolysis and inhibits protein synthesis, ultimately causing muscle atrophy.
Why this rating
Well-established mechanism in the literature reviewed.
Source
Inflammation: Roles in Skeletal Muscle Atrophy
Yanan Ji et al. · Antioxidants · 2022
DOI 10.3390/antiox11091686
narrative_reviewCited 274×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- 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.Good
- 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
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