The article discusses the role of ferroptosis, a regulated form of cell death, in various cardiac injuries and diseases. Ferroptosis is involved in ischemia/reperfusion (I/R) cardiac injury, cardiomyopathy induced by antitumor drugs, diabetes, sepsis, and stress. The activation of kinases such as AMPK, PKC, ERK1/2, PI3K, and Akt, and transcription factors like Nrf2 and STAT3, can prevent ferroptosis. In contrast, the simulation of GSK-3β contributes to ferroptosis. Non-coding RNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play a significant role in regulating ferroptosis. For example, miR-450b-5p, miR-210-3p, and miR-199a-5p can increase the tolerance of cardiomyocytes to hypoxia/reoxygenation by inhibiting ferroptosis. Circ_0091761 RNA, miR-214-3p, miR-199a-5p, miR-375-3p, miR-26b-5p, and miR-15a-5p can aggravate ferroptosis. The article also highlights the involvement of ferroptosis in I/R cardiac injury, chemotherapeutic agent-induced cardiomyopathy, septic cardiomyopathy, diabetic cardiomyopathy, and stress-induced cardiac injury. Ferroptosis inhibitors like ferrostatin-1 and liproxstatin-1 have been shown to reduce infarct size and improve cardiac function in animal models. Overall, the study emphasizes the potential of targeting ferroptosis for the development of novel drugs to prevent and treat cardiac injuries and diseases.The article discusses the role of ferroptosis, a regulated form of cell death, in various cardiac injuries and diseases. Ferroptosis is involved in ischemia/reperfusion (I/R) cardiac injury, cardiomyopathy induced by antitumor drugs, diabetes, sepsis, and stress. The activation of kinases such as AMPK, PKC, ERK1/2, PI3K, and Akt, and transcription factors like Nrf2 and STAT3, can prevent ferroptosis. In contrast, the simulation of GSK-3β contributes to ferroptosis. Non-coding RNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play a significant role in regulating ferroptosis. For example, miR-450b-5p, miR-210-3p, and miR-199a-5p can increase the tolerance of cardiomyocytes to hypoxia/reoxygenation by inhibiting ferroptosis. Circ_0091761 RNA, miR-214-3p, miR-199a-5p, miR-375-3p, miR-26b-5p, and miR-15a-5p can aggravate ferroptosis. The article also highlights the involvement of ferroptosis in I/R cardiac injury, chemotherapeutic agent-induced cardiomyopathy, septic cardiomyopathy, diabetic cardiomyopathy, and stress-induced cardiac injury. Ferroptosis inhibitors like ferrostatin-1 and liproxstatin-1 have been shown to reduce infarct size and improve cardiac function in animal models. Overall, the study emphasizes the potential of targeting ferroptosis for the development of novel drugs to prevent and treat cardiac injuries and diseases.