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Background: The existence of aberrant myocardial activity and function in the exclusion of those other cardiovascular events, such as atherosclerosis, hypertension, and severe valve disease, is known as diabetic cardiomyopathy. Diabetes patients are much more prone to death from cardiovascular illnesses than from any other cause, and they also have a 2–5 fold higher likelihood of acquiring cardiac failure and other complications. Objective: In this review, the pathophysiology of diabetic cardiomyopathy is discussed, with an emphasis on the molecular and cellular irregularities that arise as the condition progresses, as well as existing and prospective future treatments. Method: The literature for this topic was researched utilizing Google Scholar as a search engine. Before compiling the review article, several research and review publications from various publishers, including Bentham Science, Nature, Frontiers, and Elsevier, were investigated. Result: The abnormal cardiac remodelling, marked by left ventricular concentric thickening and interstitial fibrosis contributing to diastolic impairment, is mediated by hyperglycemia, and insulin sensitivity. The pathophysiology of diabetic cardiomyopathy has been linked to altered biochemical parameters, decreased calcium regulation and energy production, enhanced oxidative damage and inflammation, and a build-up of advanced glycation end products. Conclusion: Antihyperglycemic medications are essential for managing diabetes because they successfully lower microvascular problems. GLP-1 receptor agonists and sodium-glucose cotransporter 2 inhibitors have now been proven to benefit heart health by having a direct impact on the cardiomyocyte. To cure and avoid diabetic cardiomyopathy new medicines are being researched, including miRNA and stem cell therapies.