A comprehensive review of the novel therapeutic targets for the treatment of diabetic cardiomyopathy

Figures

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  Figure 1.. Schematic diagram showing different causes of diabetes-associated cardiomyopathy. AGEs, advanced glycation end products; NO, nitric oxide; RAAS, renin angiotensin aldosterone system; RAGE, receptor for advanced glycation end product; TGF-β, transforming growth factor-β.

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  Figure 2.. Mechanism contributing to impaired insulin signaling, glucotoxicity, and lipotoxicity in DCM. AGE, advanced glycation end product; Akt, protein kinase B; AP-1, activator protein 1; AS160, Akt substrate of 160 kDa; cGMP, cyclic guanosine monophosphate; DAG, diacylglycerol; DCM, diabetic cardiomyopathy; FA, fatty acid; FFA, free fatty acids; GLUT4, glucose transporter 4; GSV, GLUT4 storage vesicle; IRS, insulin receptor substrate; NF-κB, nuclear factor-κB; NO, nitric oxide; PDK1, 3-phosphoinositide-dependent kinase 1; PI3K, phosphoinositide-3-kinase; PIP2, phosphatidylinositol 4,5-bisphosphate; PIP3, phosphatidylinositol 4,5-bisphosphate; PKG, protein kinase G; PPAR, peroxisome proliferators activated receptors; ROS, reactive oxygen species; TGF-β, transforming growth factor-β.

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  Figure 3.. Schematic illustration of the role of AGEs in DCM. AGE, advanced glycation end product; Akt, protein kinase B; DCM, diabetic cardiomyopathy; JAK-STAT, Janus kinase–signal transducer and activator of transcription; MAPK, mitogen-activated protein kinase; PI3K, phosphoinositide-3-kinase; RAGE, receptor for advanced glycation end product.

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  Figure 4.. Role of FoxO proteins in DCM. Akt, protein kinase B; DCM, diabetic cardiomyopathy; FoxO, Forkhead box protein O; JAK, Janus kinase; PDK1, 3-phosphoinositide-dependent kinase; PI3K, phosphoinositide-3-kinase.