TTN and Myocardial fibrosis: Oxidative stress is not only reported to induce cardiac hypertrophy [46] and myocardial fibrosis [47], but also to increase titin-based passive stiffness [48, 49] via promoting the formation of disulfide bridges within the disordered N2-Bus element of cardiac titin, thus playing an important role in pathological progression of diastolic dysfunction.