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. 2022 Jun 28;13:927163. doi: 10.3389/fphys.2022.927163

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Copyright © 2022 Fonseca and Izar.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pivotal role of inflammation in patients with metabolic syndrome. RAS—renin angiotensin system; SNS—sympathetic nervous system; FFA—free fatty acids. Perivascular adipose tissue causes endothelial dysfunction and local inflammation, contributing for atherosclerotic plaque complications. Changes in microbiota composition and higher permeability of the intestinal mucosa to bacterial products such as lipopolysaccharides activate inflammatory pathways. Macrophages and lymphocytes infiltrate visceral adipose tissue and release proinflammatory cytokines, which are related to insulin resistance. These cytokines and FFA change cell signaling related to insulin causing endothelial dysfunction, insulin resistance, and cardiovascular remodeling. The systemic inflammatory status is also related to increased thrombotic risk, leading to ischemic events.