Irisin and the muscle–brain axis: Mechanisms and translational potential

Didn't your competent? doctor tell you this a long time ago? and got you recovered enough to do this exercise amount?

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

• irisin (12 posts to October 2013)

The latest here: 

Irisin and the muscle–brain axis: Mechanisms and translational potential

Beatrice Arosio a a,b,* , 

Anna Picca c,d Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy b c d Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy Department of Medicine and Surgery, LUM University, Casamassima, Italy Fondazione Policlinico Universitario 'A. Gemelli' IRCCS, Rome, Italy ARTICLE INFO Section Editor: Christiaan Leeuwenburgh 

Keywords: Brain-derived neurotrophic factor Cognition Myokine Neurodegeneration Neuroinflammation Oxidative stress Skeletal muscle 

ABSTRACT 

The muscle–brain axis integrates peripheral metabolic activity with central nervous system function. Among the endocrine signaling molecules regulating such crosstalk, the peptide hormone irisin released during muscle contraction seems to play relevant roles. Irisin is generated by the proteolytic cleavage of the fibronectin type III domain-containing protein 5 and has emerged as a key regulator of neurotrophic and metabolic adaptation. Although initially described as a myokine, irisin is also expressed in adipose and neural tissues, acting through autocrine, paracrine, and endocrine mechanisms. Irisin binds to the α V/β5 integrin receptor complex and activates a network of signaling pathways which promote mitochondrial biogenesis, autophagy, oxidative stress resistance, and modulation of inflammatory responses. Within the central nervous system, irisin induces brain- derived neurotrophic factor expression and contributes to synaptic plasticity, neurogenesis, and cognitive preservation. Experimental models show that irisin reduces amyloid burden, limits α-synuclein pathology, suppresses neuroinflammation, and stabilizes blood–brain barrier integrity, supporting a disease-modifying role in neurodegenerative conditions. In skeletal muscle, irisin stimulates myogenesis, enhances anabolic signaling, and improves metabolic efficiency, suggesting broader relevance for sarcopenia and age-related metabolic decline. Herein, we discuss irisin as a promising biomarker and a candidate therapeutic target for disorders characterized by concurrent muscle deterioration and cognitive impairment.