Myocardial ischemia, hypoxia and necrosis after myocardial infarction lead to a multiphase repair process in which damaged tissue is replaced with fibrous scars produced by fibroblasts and myofibroblasts. Non-infarct ventricular wall reactive remodeling, including interstitial and perivascular fibrosis, leads to changes in ventricular wall geometry, biomechanics, biochemistry and so on. Although initial repair fibrosis is essential to prevent ventricular wall rupture, excessive fibrosis leads to progressive damage to heart function and eventually to heart failure. Recent studies have shown that the heart has plasticity, restoring impaired cardiac function, and promoting myocardial repair after infarction are important targets for the treatment of cardiovascular diseases. To this end, people continue to explore new therapies, regeneration therapy for myocardial infarction treatment has brought new hope. This review summarizes the current myocardial infarction repair and reaction mechanism of cardiacl fibrosis, to explore the potential of inducing fibroblasts and myofibroblasts into cardiomtocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis.