Thus, further investigations are needed to understand the mechanisms to restore cardiac Ca 2+ homeostasis and function, and to serve as potential therapeutic targets in the treatment of DCM.ĭiabetic cardiomyopathy (DCM) is one of the end-stage consequences of mortality and morbidity in patients with diabetes mellitus. Inflammatory mediators, miRNA and exosomes are shown to interact with these regulators, however how these mediators are linked to Ca 2+ handling during DCM pathogenesis remains elusive. In this literature review, we have demonstrated that Ca 2+ regulators are tightly controlled at different molecular and cellular levels during various biological processes in the heart.

Inflammatory response and Ca 2+ signaling are interrelated and DCM has been known to adversely affect many of these signaling molecules either qualitatively and/or quantitatively. Furthermore, the complex pathophysiology of DCM is linked with exosomes, which has recently shown to facilitate intercellular (cell-to-cell) communication through biomolecules such as micro RNA (miRNA), proteins, enzymes, cell surface receptors, growth factors, cytokines, and lipids. Although the existence of DCM was established nearly four decades ago, the exact mechanisms underlying this disease pathophysiology is constantly evolving. Inflammation, changes in calcium (Ca 2+) handling and cardiomyocyte loss are often implicated in the development and progression of DCM. Diabetic cardiomyopathy (DCM) often manifests as reduced cardiac contractility, myocardial fibrosis, diastolic dysfunction, and chronic heart failure.

Diabetes mellitus is one of the prime risk factors for cardiovascular complications and is linked with high morbidity and mortality.

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