The Role of the Notch Signaling Pathway in Recovery of Cardiac Function after Myocardial Infarction

Myocardial infarction (MI) is a pathological process, evidencing as massive death of cardiomyocytes associated with hypoxic and oxidative stress. The formation of areas of fibrosis ultimately leads to heart failure. There are some mechanisms that contribute to the functional repair of the heart. In most mammals, including humans, the Notch signaling pathway has cardioprotective effects. It is involved in the formation of the heart in embryogenesis and in the restoration of cardiac function after MI due to: (1) reducing oxidative stress; (2) prevention of apoptosis; (3) regulation of inflammation; (4) containment of fibrosis and hypertrophy of cardiomyocytes; (5) tissue revascularization; and (6) regulation of proliferation and differentiation of cardiomyocytes. In addition, the Notch signaling pathway interacts with other signaling cascades involved in the pathogenesis of MI and subsequent cardiac repair. In this review, we consider the Notch signaling pathway as a potential target for therapeutic approaches aimed at improving cardiac recovery after MI.

Automated summary

The Notch signaling pathway plays a cardioprotective role in heart development and recovery after myocardial infarction by reducing oxidative stress, preventing apoptosis, regulating inflammation, containing fibrosis and hypertrophy, promoting tissue revascularization, and regulating proliferation and differentiation of cardiomyocytes. It interacts with other signaling cascades involved in the pathogenesis and repair of myocardial infarction.