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Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity

ABSTRACT: Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity

PROVIDER: PRJNA592555 | ENA |

REPOSITORIES: ENA

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Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity

Project description:To investigate the function and potential mechanism of PARP-1 poly(ADP-ribose) polymerase 1 (PARP1) in diabetic neointimal hyperplasia. Type 1 diabetes mellitus was induced using streptozotocin (STZ) in wild-type mice and PARP1-/- mice, and ligation of the left carotid artery was performed to induce neointimal hyperplasia. Ligated carotid arteries from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation and migration than arteries from nondiabetic mice. The augmented remodeling response was absent in diabetic mice deficient in PARP1. PARP1 deficiency reduces diabetic neointimal hyperplasia by upregulating tissue factor pathway inhibitor (TFPI)-2, which acted as a suppressor of vascular smooth muscle cell (VSMCs) proliferation and migration. The underlying mechanisms involve PARP1 that acts as a negative transcription factor by enhancing TFPI-2 promoter DNA methylation. Our studies demonstrated for the first time that Inhibition of PARP1 alleviates neointimal hyperplasia in diabetes by up-regulating TFPI-2 expression and blocking VSMC proliferation and migration. The development of PARP1 inhibitors might serve to limit mainly proliferative and migratory processes in restenosis-prone diabetic patients

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Deletion of hyaluronan synthase 3 inhibits neointimal hyperplasia

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Project description:Neointimal hyperplasia (NIH) are the major causes of re-stenosis in coronary intervention. Fibroblasts, vascular smooth muscle cells and endothelial cells are the main disease-causing cells in NIH. However, Yet how these cells contribute to the pathophysiology of NIH remains elusive. This study was aimed at gaining new insights into the heterogeneity of these cells by using single-cell RNA sequencing and up-to-date analytical method.

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Novel Roles of Nrf3-Trim5 Axis in Vascular Smooth Muscle Cell Dysfunctions and Neointimal Hyperplasia

Project description:Neointimal hyperplasia (NIH), driven by vascular smooth muscle cell (VSMC) dysfunction, is a key factor in vascular diseases like atherosclerosis and restenosis. While Nrf3 is known to regulate VSMC differentiation, its role in NIH remains unclear. Using transcriptomic data, Nrf3 knockout mice (global), we assessed Nrf3’s impact on VSMC function and NIH. We identified Trim5, a gene linked to coronary artery disease, as a downstream target of Nrf3, which promotes autophagy in VSMCs and injured arteries, enhancing VSMC dysfunction and NIH. Nrf3 overexpression increased VSMC proliferation, migration, and inflammation, while deletion or knockdown had the opposite effects. Nrf3-/- and Nrf3ΔSMC mice showed reduced VSMC accumulation and attenuated NIH after vascular injury. These findings highlight Nrf3 as a novel modulator of VSMC dysfunction and injury-induced NIH, with potential for therapeutic targeting of the Nrf3-Trim5 axis to treat NIH-related vascular diseases.

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