Since Ranolazine approval as an antianginal medication by the US Food and Drug Administration in 2006, it has been administered to specific patient populations with stable angina. Originally, it was thought that ranolazine's therapeutic actions were due to its inhibition of the metabolism of fatty acids. However, as research progressed, it became clear that ranolazine's primary advantageous benefits come from its influence on the heart's late sodium current. Numerous experimental and clinical studies have tested ranolazine either directly or indirectly on heart failure since late-sodium currents have been found to be involved in various heart pathologies such as ischemia, arrhythmias, systolic and diastolic dysfunctions, and all these conditions are associated with heart failure. The inhibition of the underlying mechanisms of cardiac remodeling, such as ion disruptions, oxidative stress, inflammation, apoptosis, fibrosis, metabolic dysregulation, and neurohormonal dysfunction, by ranolazine is reviewed after any kind of severe injury, along with open questions. Ranolazine additional metabolic properties contribute to its efficacy in treating conditions other than coronary artery disease. Our publication will focus on potential therapeutic applications of ranolazine, extending beyond cardiology.