COL1A1 and infarction: The decreased ratio between COL3A1 and COL1A1 expression suggested that, in all conditions, there was a superior accumulation of new Collagen Type I respect to Collagen Type III (Figure 2f), which is typical hallmark of the last stages of post‐infarction cardiac fibrosis, as highlighted in previous studies and in clinical reports.[18] The role of both TGF‐β1 and mechanical stretching in triggering ECM production was also confirmed by the analysis of deposited Collagen Type I, Fibronectin and Aggrecan proteins (Figure 3).