Research

Hormonal

Central nervous system (CNS) inflammation, specifically via IL-1β signaling, induces skeletal muscle atrophy through the activation of the hypothalamic-pituitary-adrenal (HPA) axis and subsequent glucocorticoid release, independent of direct peripheral cytokine action on muscle.

In chronic inflammatory conditions, muscle loss is driven significantly by the brain's response to inflammation (via the HPA axis and stress hormones), not just by the inflammation hitting the muscle directly. This suggests that interventions targeting the central inflammatory response or stress hormone pathways may be necessary to prevent muscle wasting, rather than just focusing on local muscle nutrition or exercise.

GoodSupportsHIGH confidence
We demonstrate that central nervous system (CNS)–delimited interleukin 1β (IL-1β) signaling alone can evoke a catabolic program in muscle, rapidly inducing atrophy. This effect is dependent on hypothalamic–pituitary–adrenal (HPA) axis activation, as CNS IL-1β–induced atrophy is abrogated by adrenalectomy.
Theodore P. Braun et al. · The Journal of Experimental Medicine · 2011

Why this rating

High-quality mechanistic evidence using multiple animal models (mice and rats), genetic knockouts (MC4RKO), surgical interventions (adrenalectomy), and pharmacological blockade, though results are not directly translatable to humans without further study.

Source

Central nervous system inflammation induces muscle atrophy via activation of the hypothalamic–pituitary–adrenal axis

Theodore P. Braun et al. · The Journal of Experimental Medicine · 2011

DOI 10.1084/jem.20111020

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DOI resolved against Crossref · corpus check 2026-06-10

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