Crosstalk between perivascular adipose tissue and adipocyte-derived peptide in the pathogenesis of diabetic cardiomyopathy

Abstract

Diabetic cardiomyopathy (DCM) is a prevalent complication in diabetic patients, and its pathogenic mechanism involves multiple endocrine and metabolic factors, with dyslipidemia playing a pivotal role in the pathogenesis of the disease. Recent studies have highlighted the importance of peptides in energy metabolism and their potential effect on the onset and development of DCM by affecting the function of perivascular adipose tissue (PVAT). The present review aims to examine the effect of these peptides on perivascular adipose tissue and myocardial metabolism during the pathogenesis of DCM, focusing on the role of peptides distributed in perivascular adipose tissue in cardioprotection and their underlying mechanisms of action. In addition, we will explore future research directions and potential clinical applications of these peptides in the treatment of DCM.

Keywords: Diabetic cardiomyopathy; Peptides; Perivascular adipose tissue.

Fig. 1

The effects of apelin on perivascular adipose tissue. APJ, Apelin Receptor;TNFα, tumor necrosis factor α; IL, interleukin; PPAR, peroxisome proliferators-activated receptors; C/EBPα, CCAAT/enhancer binding proteins α; AMPK, Adenosine 5’-monophosphate (AMP)-activated protein kinase; PI3K, phosphatidylinositol-3-kinase;Akt, protein kinase B

Fig. 2

The effects of apelin on vascular endothelium and myocardium. APJ, Apelin Receptor;NO, nitric oxide; TNFα, tumor necrosis factor α; IL, interleukin; CPT-1, carnitine palmityl transferase I; TGF-β, transforming growth factor-β; eNOS, endothelial nitric oxide synthase; AMPK, adenosine 5’-monophosphate (AMP)-activated protein kinase

Fig. 3

The effects of spexin on perivascular adipose tissue. IL, interleukin; UCP1, uncoupling protein 1; M1a, Macrophages 1a; M1b, Macrophages 1b; M2, Macrophages 2;TBX1, T-box 1; CIDEA, Cell Death-Inducing DNA Fragmentation Factor Alpha-like Effector A

Fig. 4

The effects of spexin on vascular endothelium and myocardium. UCP2, uncoupling protein 2; CPT-1, carnitine palmityl transferase I; ROS, Reactive Oxygen Species; ATP, Adenosine triphosphate

Fig. 5

The effects of galanin on perivascular adipose tissue. IL, interleukin; Gal1R, Galanin Receptor 1; Gal2R, Galanin Receptor 2; TNFα, tumor necrosis factor α; ROS, Reactive Oxygen Species; GLUT4, Glucose Transporter Type 4; Akt, protein kinase B

Fig. 6

The effects of galanin on vascular endothelium and myocardium. M1, Macrophages 1; M2, Macrophages 2; TNFα, tumor necrosis factor α; IL, interleukin; PI3K, phosphatidylinositol-3-kinase; Akt, protein kinase B; GLUT4, glucose transporter type 4; I/R injure, ischemia reperfusion injury; ROS, reactive oxygen species; Akt, protein kinase B

Fig. 7

The effects of GALP on perivascular adipose tissue and vascular endothelium and myocardium. IL, interleukin; UCP1, uncoupling protein 1; GLUT4, Glucose Transporter Type 4;GNG, gluconeogenesis

Fig. 8

The common molecular pathways of perivascular adipose tissue-related peptide in regulating cardiomyocytes. PVAT, perivascular adipose tissue; APJ, Apelin Receptor; Gal1R, Galanin Receptor 1;Gal2R, Galanin Receptor 2; IL, interleukin; TNFα, tumor necrosis factor α; PI3K, phosphatidylinositol-3-kinase;Akt, protein kinase B; PPAR, peroxisome proliferators-activated receptors; C/EBPα, CCAAT/enhancer binding proteins α; AMPK, Adenosine 5’-monophosphate (AMP)-activated protein kinase;;NO, nitric oxide; TGF-β, transforming growth factor-β; eNOS, endothelial nitric oxide synthase; UCP1, uncoupling protein 1; M1a, Macrophages 1a; M1b, Macrophages 1b; M2, Macrophages 2;TBX1, T-box 1; CIDEA, Cell Death-Inducing DNA Fragmentation Factor Alpha-like Effector A; ROS, Reactive Oxygen Species; ATP, Adenosine triphosphate; GLUT4, Glucose Transporter Type 4;;I/R injure, ischemia reperfusion injury; GNG, gluconeogenesis