Pathophysiological Role of Adiponectin, Leptin and Asymmetric Dimethylarginine in the Process of Atherosclerosis

Abstract

Adipose tissue is recognized as a rich source of proinflammatory mediators that may directly contribute to vascular injury, insulin resistance, and atherogenesis. Many studies have shown that adiponectin has antiatherogenic and anti-inflammatory properties. Adiponectin acts not only as a factor increasing insulin sensitivity, and the protective effect may result from its ability to suppress production of proinflammatory cytokines. It negatively regulates the expression of TNF-alpha and C-reactive protein (CRP) in adipose tissue; reduces expression of vascular and intracellular adhesion molecules (VCAM-1, ICAM-1), E-selectin, interleukin-8 (IL-8). Hyperleptinemia has been linked with the development of hypertension and endothelial dysfunction/atherosclerosis, two main pathophysiological conditions associated with cardiovascular disease development. Leptin-mediated increases in sympathetic nervous system activity may be among the principal mechanisms evoking obesity related hypertension. Leptin stimulates the secretion of proinflammatory cytokines, and increases the release of endothelin-1 (ET-1), which may promote hypertension. Increased serum levels of asymmetric dimethylarginine (ADMA), a physiological regulator of the biosynthesis of nitric oxide (NO), promote the process of atherosclerosis, leading to the occurrence of endothelial dysfunction and cardiovascular disease.

Association of Serum Leptin and Adiponectin Concentrations with Type 2 Diabetes Biomarkers and Complications Among Saudi Women

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Association of Serum Leptin and Adiponectin Concentrations with Type 2 Diabetes Biomarkers and Complications Among Saudi Women

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Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia

“…NO is mainly catalyzed and produced by eNOS, which has the function of vasodilatation and protecting vascular endothelium under physiological contents [ 25 , 26 ]. Accumulating evidence has suggested that intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), endothelin 1 (ET-1), and E-selectin play pivotal roles in the mechanisms of endothelial dysfunction [ 27 , 28 ]. In the present study, the expression of ICAM-1, VCAM-1, ET-1, and E-selectin was upregulated and the levels of NO and eNOS were downregulated in HUVECs cultured with culture medium of hypoxic JEG-3 cells.…”

The Critical Roles of Methyltransferase‐Like 3 in Atherosclerosis and Arterial Infarction: Breakthroughs in Mechanism Understanding

“…Collectively, these findings suggest that METTL3 facilitates endothelial atherogenic progression through m 6 Adependent stabilisation of EGFR mRNA (Figure 1). Oxidised low-density lipoprotein (ox-LDL) deposition in the vascular endothelium is one main cause of AS, which damages vascular EC and leads to the accumulation of lipids and M1 inflammatory macrophage in the damaged area, thereby forming AS plaques [21,22]. Research indicates that ox-LDL triggers EC activation and dysfunction via multiple mechanisms that are likely associated with METTL3.…”

Association of Serum Leptin and Adiponectin Concentrations with Type 2 Diabetes Biomarkers and Complications Among Saudi Women

“……”

Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia

“…NO is mainly catalyzed and produced by eNOS, which has the function of vasodilatation and protecting vascular endothelium under physiological contents [ 25 , 26 ]. Accumulating evidence has suggested that intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), endothelin 1 (ET-1), and E-selectin play pivotal roles in the mechanisms of endothelial dysfunction [ 27 , 28 ]. In the present study, the expression of ICAM-1, VCAM-1, ET-1, and E-selectin was upregulated and the levels of NO and eNOS were downregulated in HUVECs cultured with culture medium of hypoxic JEG-3 cells.…”

The Critical Roles of Methyltransferase‐Like 3 in Atherosclerosis and Arterial Infarction: Breakthroughs in Mechanism Understanding

“…Collectively, these findings suggest that METTL3 facilitates endothelial atherogenic progression through m 6 Adependent stabilisation of EGFR mRNA (Figure 1). Oxidised low-density lipoprotein (ox-LDL) deposition in the vascular endothelium is one main cause of AS, which damages vascular EC and leads to the accumulation of lipids and M1 inflammatory macrophage in the damaged area, thereby forming AS plaques [21,22]. Research indicates that ox-LDL triggers EC activation and dysfunction via multiple mechanisms that are likely associated with METTL3.…”

Association of Serum Leptin and Adiponectin Concentrations with Type 2 Diabetes Biomarkers and Complications Among Saudi Women

“……”

Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia

“…NO is mainly catalyzed and produced by eNOS, which has the function of vasodilatation and protecting vascular endothelium under physiological contents [ 25 , 26 ]. Accumulating evidence has suggested that intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), endothelin 1 (ET-1), and E-selectin play pivotal roles in the mechanisms of endothelial dysfunction [ 27 , 28 ]. In the present study, the expression of ICAM-1, VCAM-1, ET-1, and E-selectin was upregulated and the levels of NO and eNOS were downregulated in HUVECs cultured with culture medium of hypoxic JEG-3 cells.…”

The Critical Roles of Methyltransferase‐Like 3 in Atherosclerosis and Arterial Infarction: Breakthroughs in Mechanism Understanding

“…Collectively, these findings suggest that METTL3 facilitates endothelial atherogenic progression through m 6 Adependent stabilisation of EGFR mRNA (Figure 1). Oxidised low-density lipoprotein (ox-LDL) deposition in the vascular endothelium is one main cause of AS, which damages vascular EC and leads to the accumulation of lipids and M1 inflammatory macrophage in the damaged area, thereby forming AS plaques [21,22]. Research indicates that ox-LDL triggers EC activation and dysfunction via multiple mechanisms that are likely associated with METTL3.…”