The loss of tissue integrity disturbs the crosslinked ECM framework, allowing mechanical cues to promote the transition.[305] The secretory phenotype of myofibroblasts includes type 1 collagen, TGF‐β, and α‐SMA, which promote the transdifferentiation of other cells to myofibroblasts.[87] Angiotensin II, which can also be secreted by cardiac myofibroblasts, facilitates the production of the ECM through TGF‐β or type I angiotensin receptor (AT1R).[306, 307] In addition, systemic extracardiac profibrotic alterations, such as diabetes and CKD, facilitate cardiac fibrosis. Here, TGFB1 is linked to diabetes mellitus.