SMAD2 and chronic obstructive pulmonary disease: Both myostatin and growth differentiation factor 15 (GDF‐15) are elevated in a range of muscle wasting conditions and are able to promote atrophy.14, 15, 16 Myostatin promotes muscle wasting by activating the canonical TGF‐β signalling pathway via phosphorylation of SMAD proteins, leading to increased protein breakdown and autophagy.17, 18 SMAD2/3 can also be activated in the absence of exogenous ligand by miR‐542‐5p, a miRNA quadriceps expression of which is positively associated with lung disease severity in patients with COPD.19