Doxorubicin， an anthracycline antitumor drug， is one of the most effective anticancer drugs in clinical practice. However， it can cause changes in cardiac function and damage to other organs. Since cardiomyocytes are difficult to divide and proliferate， most injuries are irreversible， and it is difficult to reverse the influence on cardiac function. The heart is involved in a relatively high oxidative metabolism and a relatively low level of antioxidant defense， which makes it sensitive to damage caused by free radicals. Doxorubicin can lead to dose-dependent cardiomyopathy and congestive heart failure， and even cognitive dysfunction （loss of memory and attention， difficulty to perform multitasking）. And doxorubicin-induced dose-dependent cardiomyopathy can lead to significant hypotension， tachycardia， dilatation of the heart， and heart failure. Therefore， it is of great value to investigate the mechanism of action of doxorubicin in cardiotoxicity. Many studies have attempted to describe and elucidate the mechanism of its cardiotoxic effects. Although there have been abundant data covering a wide range of drug-mediated effects， the exact mechanism remains controversial. Many studies have found that mitochondria are the main targets of doxorubicin-induced oxidative stress， both in acute and chronic treatments. This article reviews the molecular mechanism of action of doxorubicin in cardiotoxicity through mitochondrial injury.