This cascade initially leads to cellular stress, which can significantly impact vascular permeability, promoting the degeneration of cells in myocardial capillaries [41] and subsequently, myocardial hypertrophy and fibrosis (significant positive correlation with ST2/IL-33R) (Figure 1C) [27], followed by an increase in myocardial wall stress and stretch (significant positive correlation with NT-proBNP) (Figure 1A) [21], and finally, cardiomyocyte necrosis and damage (significant positive correlation with cTn I) (Figure 1B) [19]. This evidence concerns the gene TNNI3 and cardiac hypertrophy.