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Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1.
J Mater Sci Mater Med
January 2025
Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, PR China.
In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC proliferation may be an attractive approach for preventing in-stent restenosis.
View Article and Find Full Text PDFBone marrow-derived NGFR-positive dendritic cells regulate arterial remodeling.
Am J Physiol Cell Physiol
February 2025
Department of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
It has been proposed that bone marrow contributes to the pathogenesis of arteriosclerosis. Nerve growth factor receptor (NGFR) is expressed in bone marrow stromal cells; it is also present in peripheral blood and ischemic coronary arteries. We hypothesized that bone marrow-derived NGFR-positive (NGFR) cells regulate arterial remodeling.
View Article and Find Full Text PDFFhl1, a new spatially specific protein, regulates vein graft neointimal hyperplasia.
Clin Transl Med
December 2024
Department of Cardiac Surgery, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Article Synopsis
- Vein grafts are critical for treating coronary artery disease, but neointimal hyperplasia (NIH) poses a significant challenge to their long-term success, with current identification and intervention methods being insufficient.
- Researchers conducted a study using rats to observe the NIH development process after vein grafting while examining gene expression and specific markers related to NIH through various analytical methods.
- The results showed that repair cells from outside the graft contribute significantly to NIH, with the protein Fhl1 playing a protective role against inflammation and cell proliferation, offering potential targets for improved treatments.
Empagliflozin Attenuates Neointima Formation After Arterial Injury and Inhibits Smooth Muscle Cell Proliferation and Migration by Suppressing Platelet-Derived Growth Factor-Related Signaling.
J Am Heart Assoc
November 2024
Division of Cardiology, Department of Internal Medicine, Taipei Veterans General Hospital National Yang Ming Chiao Tung University College of Medicine Taipei Taiwan.
Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce cardiovascular events. However, the precise mechanisms beyond glycemic control are not fully understood. The objective of this study was to determine the role of PDGF (platelet-derived growth factor)-related signaling in empagliflozin-mediated inhibition of neointima formation.
View Article and Find Full Text PDFmA Modification of Profilin-1 in Vascular Smooth Muscle Cells Drives Phenotype Switching and Neointimal Hyperplasia via Activation of the p-ANXA2/STAT3 Pathway.
Arterioscler Thromb Vasc Biol
December 2024
Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, China.
Background: In-stent restenosis is characterized by a significant reduction in lumen diameter within the stented segment, primarily attributed to excessive proliferation of vascular smooth muscle cells (VSMCs) and neointimal hyperplasia. PFN1 (profilin-1), an actin-sequestering protein extensively studied in amyotrophic lateral sclerosis, remains less explored in neointimal hyperplasia.
Methods: Utilizing single-cell RNA sequencing alongside data from in-stent restenosis patients and various experimental in-stent restenosis models (swine, rats, and mice), we investigated the role of PFN1 in promoting VSMC phenotype switching and neointimal hyperplasia.
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