cardiovascular-agents and Metabolism--Inborn-Errors

The landmark discoveries of leptin and adiponectin firmly established adipose tissue as a sophisticated and highly active endocrine organ, opening a new era of investigating adipose-mediated tissue crosstalk. Both obesity-associated hyperleptinemia and hypoadiponectinemia are important biomarkers to predict cardiovascular outcomes, suggesting a crucial role for adiponectin and leptin in obesity-associated cardiovascular disorders. Normal physiological levels of adiponectin and leptin are indeed essential to maintain proper cardiovascular function. Insufficient adiponectin and leptin signaling results in cardiovascular dysfunction. However, a paradox of high levels of both leptin and adiponectin is emerging in the pathogenesis of cardiovascular disorders. Here, we (1) summarize the recent progress in the field of adiponectin and leptin and its association with cardiovascular disorders, (2) further discuss the underlying mechanisms for this new paradox of leptin and adiponectin action, and (3) explore the possible application of partial leptin reduction, in addition to increasing the adiponectin/leptin ratio as a means to prevent or reverse cardiovascular disorders.

Topics: Adiponectin; Adipose Tissue; Animals; Anti-Obesity Agents; Bariatric Surgery; Cardiovascular Agents; Cardiovascular Diseases; Cardiovascular System; Humans; Leptin; Metabolism, Inborn Errors; Obesity; Signal Transduction

Restenosis is a pathologic re-narrowing of a coronary artery lesion after mechanical injury. Its pathophysiological mechanisms have not been fully elucidated at present, but are thought to include inflammation, vascular smooth muscle cell (VSMC) proliferation, and matrix remodeling, beginning with insufficient endothelium healing. Restenosis presents with angina symptoms or acute coronary syndromes and lead to a revascularization, either with coronary artery bypass or repeat percutaneous coronary intervention. Some studies have reported that hypoadiponectinemia has been an independent risk factor for the onset of acute coronary syndromes and restenosis. Accumulating evidence shows that low concentrations of adiponectin may be involved in impairing endothelium functions, inflammation, and VSMC proliferation that lead to restenosis. Preclinical studies have proven that adiponectin promotes endothelium healing, effectively inhibits inflammation, and maintains contractile phenotypes of VSMCs, indicating that it may be developed as a new therapeutic target for the treatment of restenosis.

Topics: Adiponectin; Animals; Cardiovascular Agents; Cell Proliferation; Coronary Restenosis; Drug Delivery Systems; Humans; Metabolism, Inborn Errors; Muscle, Smooth, Vascular; Treatment Outcome