Why the study?
Myocardial ischemia in diabetes is accompanied by impaired angiogenesis, and understanding these mechanisms in experimental models is needed to develop novel therapeutic strategies for diabetic ischemic heart disease.
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This review summarizes the structural and molecular mechanisms of impaired myocardial angiogenesis in experimental diabetes, highlighting potential targets for therapeutic strategies.
Diabetes mellitus (DM) represents one of the most significant global health challenges, not only due to its metabolic derangements but also because of its strong association with cardiovascular diseases. Myocardial ischemia in the diabetic heart is accompanied by profound alterations in angiogenesis, impairing tissue perfusion and regenerative responses. Experimental models of diabetes, including chemical induction and genetic approaches, have provided important insights into the structural and molecular mechanisms underlying impaired myocardial angiogenesis. This article reviews the morphological and molecular features of myocardial angiogenesis in experimental diabetes, focusing on endothelial dysfunction, alterations in capillary density, ultrastructural damage, and dysregulation of signaling pathways such as VEGF, HIF-1α, and PI3K/Akt. Understanding these mechanisms is crucial for the development of novel therapeutic strategies to improve myocardial recovery in diabetic ischemic heart disease.
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Dilnoza Khusanbayovna Kurbanova (2025) studied this question.
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