Diabetic cardiomyopathy, a significant microvascular complication of diabetes, is primarily characterized by myocardial fibrosis and functional abnormalities. Chronic hyperglycemia plays a key role in this condition by initiating the activation and recruitment of immune cells, triggering inflammatory cascades that contribute to both systemic and localized cardiac inflammation.
Recent studies have emphasized the pivotal role of the immune system in the development and progression of diabetic cardiomyopathy. Immune cells, which serve as the primary mediators of inflammation, are consistently present in cardiac tissue and are recruited in response to pathological hyperglycemia. The imbalance towards proinflammatory immune cells, along with elevated levels of proinflammatory cytokines, promotes fibroblast proliferation, phenotypic changes, and collagen production. These processes ultimately lead to cardiac fibrosis and hypertrophy.
Furthermore, the degree of cardiac fibrosis is closely linked to the various immune cell phenotypes and their alterations. These include cells involved in innate immunity such as macrophages, dendritic cells, mast cells, neutrophils, and natural killer cells, as well as those in adaptive immunity, including CD4+ T lymphocytes, CD8+ T lymphocytes, and B lymphocytes.
This review consolidates current understanding of the immune system’s critical involvement in the progression of diabetic cardiomyopathy. It also discusses emerging preclinical and clinical strategies targeting immune mechanisms and their potential for translational applications in the treatment of this condition.
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