TNF α and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in Hypertension and Atherosclerosis.

TNFα and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in Hypertension and Atherosclerosis. Am J Hypertens. 2020 Jun 05;: Authors: Lamb FS, Choi H, Miller MR, Stark RJ Abstract Hypertension and atherosclerosis, the predecessors of stroke and myocardial infarction, are chronic vascular inflammatory reactions. Tumor necrosis factor alpha (TNFα), the "master" pro-inflammatory cytokine, contributes to both the initiation and maintenance of vascular inflammation. TNFα induces reactive oxygen species (ROS) production which drives the redox reactions that constitute "ROS signaling". However, these ROS may also cause oxidative stress which contributes to vascular dysfunction. Mice lacking TNFα or its receptors are protected against both acute and chronic cardiovascular injury. Humans suffering from TNFα-driven inflammatory conditions such as rheumatoid arthritis and psoriasis are at increased cardiovascular risk. When treated with highly specific biologic agents that target TNFα signaling (Etanercept etc.) they display marked reductions in that risk1. The ability of TNFα to induce endothelial dysfunction, often the first step in a progression towards serious vasculopathy, is well recognized and has been reviewed elsewhere2,3. However, TNFα also has profound effects on vascular smooth muscle cells (VSMCs) including a fundamental change from a contractile to a secretory phenotype. This...
Source: American Journal of Hypertension - Category: Cardiology Authors: Tags: Am J Hypertens Source Type: research

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