Key result
Adipose tissue dysfunction in obesity leads to an altered secretion of adipokines, such as decreased adiponectin and increased TNFα, IL-6, MCP-1, and leptin, which promotes insulin resistance and atherosclerosis.
This review highlights the role of adipokines in the inflammatory pathways linking diabetes and atherosclerosis, suggesting potential therapeutic targets.
Adipokines may link inflammation across diabetes and CVD; leaves open targeted interventions pending prospective trials.
Cardiovascular diseases can be considered the most important cause of death in diabetic population and diabetes can in turn increase the risk of cardiovascular events. Inflammation process is currently recognized as responsible for the development and maintenance of diverse chronic diseases, including diabetes and atherosclerosis. Considering that adipose tissue is an important source of adipokines, which may present anti and proinflammatory effects, the aim of this review is to explore the role of the main adipokines in the pathophysiology of diabetes and atherosclerosis, highlighting the therapeutic options that could arise from the manipulation of these signaling pathways both in humans and in translational models.
No takes yet. Share an insight, caveat, or question.
Freitas‐Lima et al. (2015) conducted a review in Diabetes and atherosclerosis. Adipokines (adiponectin, TNFα, IL-6, MCP-1, leptin) was evaluated. Adipose tissue dysfunction in obesity leads to an altered secretion of adipokines, such as decreased adiponectin and increased TNFα, IL-6, MCP-1, and leptin, which promotes insulin resistance and atherosclerosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: