In our current studies, we tried to prove one of the possible mechanisms (our central hypothesis) that myocardium could secret Galectin-3 under the stimulation of myocardial stretch (or pressure overload) and the secreted Galectin-3 (in plasma or within myocardium) may in turn trigger myocardial fibrosis, which results in diastolic dysfunction or HFPEF (see Fig. 5 for the schematic presentation of our central hypothesis). This evidence concerns the gene LGALS3 and Myocardial fibrosis.