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Ai-Dong Chen

Researcher at Nanjing Medical University

Publications -  16
Citations -  428

Ai-Dong Chen is an academic researcher from Nanjing Medical University. The author has contributed to research in topics: Vascular smooth muscle & Angiotensin II. The author has an hindex of 11, co-authored 16 publications receiving 312 citations. Previous affiliations of Ai-Dong Chen include Wannan Medical College.

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Angiotensin AT1 receptors in paraventricular nucleus contribute to sympathetic activation and enhanced cardiac sympathetic afferent reflex in renovascular hypertensive rats.

TL;DR: Results indicate that the increased activity of AT1 receptors in the PVN contributes to the enhanced CSAR and excessive sympathetic activation in renovascular hypertensive rats.
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Paraventricular nucleus is involved in the central pathway of cardiac sympathetic afferent reflex in rats

TL;DR: Results indicate that inhibition or lesion of the PVN abolishes the CSAR, but excitation of the neurons in the PV N enhances the CSar, suggesting that the PVn is an important component of the central neurocircuitry of the CS AR.
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Long-term administration of tempol attenuates postinfarct ventricular dysfunction and sympathetic activity in rats

TL;DR: The normalization of the CSAR, levels of superoxide anions and AT1 receptor expression, and the response to angiotensin II in the paraventricular nucleus and rostral ventrolateral medulla may partially contribute to the beneficial effects of tempol on central sympathetic control.
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FNDC5 inhibits foam cell formation and monocyte adhesion in vascular smooth muscle cells via suppressing NFκB-mediated NLRP3 upregulation

TL;DR: Results indicate that FNDC5 inhibits oxLDL-induced foam cell formation and monocyte adhesion in VSMCs via suppressing NFκB-mediated NLRP3 upregulation and IL-1β production.
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FNDC5 Attenuates Oxidative Stress and NLRP3 Inflammasome Activation in Vascular Smooth Muscle Cells via Activating the AMPK-SIRT1 Signal Pathway.

TL;DR: It is indicated that F NDC5 deficiency aggravates while exogenous FNDC5 alleviates the Ang II-induced vascular oxidative stress and NLRP3 inflammasome activation via the AMPK-SIRT1 signal pathway in VSMCs.