We also showed that LC3β punctate staining co-localized with vimentin (a mesenchymal marker – see Figure 3e), ED-A fibronectin (Figure 3f) and phosphorylated Smad2 (Figure 3g – wherein Smad2 phosphorylation is a marker of canonical TGF-β1 activation), which supports our hypothesis about the role of autophagy and TGF-β1 in fibrosis induction in MI tissue. The gene discussed is VIM; the disease is myocardial infarction.