Current strategies to lower the incidence of ISR (in-stent restenosis) following PCI (percutaneous coronary intervention) are aimed at modifying arterial healing after stent injury. This can impair endothelial recovery and render the vessel prone to acute thrombosis. As early restoration of endothelial integrity inhibits neointimal growth and thrombosis, alternative approaches which encourage this process may provide a more effective long-term result after PCI. Oxidative stress is enhanced after PCI and participates in the regulation of endothelial regeneration and neointimal growth. Moreover, evidence suggests antioxidants improve re-endothelialization and inhibit ISR. By promoting, rather than blocking, the healing process, antioxidant and other therapies may offer an alternative or additional approach over the antiproliferative approaches common to many current devices.
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http://dx.doi.org/10.1042/CS20070207 | DOI Listing |
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 PDFRegen Biomater
December 2024
Institute of Biomedical Engineering, College of Medicine, Southwest Jiaotong University, Chengdu, Sichuan 610031, China.
Modification of polylactic acid (PLA) is a promising strategy for the next generation of bioresorbable vascular stent biomaterials. With this focus, FeMOFs nanoparticles was incorporated in PLA, and then post loading of carbon monoxide (CO) was performed by pressurization. It showed FeMOFs incorporation increased hydrophilicity of the surface and CO loading, and CO release was sustained at least for 3 days.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
January 2025
Department of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, 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 PDFBiochem Biophys Res Commun
January 2025
Department of Cardiology, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Hebei, China; Hebei Key Laboratory of Heart and Metabolism, Shijiazhuang, 050031, Hebei, China. Electronic address:
We aim to explore the impact of Proprotein convertase subtilisin-kexin type 9 (PCSK9) and its inhibitor evolocumab on neointimal hyperplasia. Wild type and PCSK9 knockout (PCSK9) mice were subjected to ligation of the common carotid artery, with or without subcutaneous injection of evolocumab. Mouse aortic vascular smooth muscle (MOVAS) cells were pretreated with evolocumab or under siRNA-mediated suppression of PCSK9, and then exposed to platelet-derived growth factor type BB(PDGF-BB), a major promoter of MOVAS transformation to a proliferative phenotype.
View Article and Find Full Text PDFbioRxiv
November 2024
Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Background: The Rho kinases 1 and 2 (ROCK1/2) are serine-threonine specific protein kinases that control actin cytoskeleton dynamics. They are expressed in all cells throughout the body, including cardiomyocytes, smooth muscle cells and endothelial cells, and intimately involved in cardiovascular health and disease. Pharmacological ROCK inhibition is beneficial in mouse models of hypertension, atherosclerosis, and neointimal thickening that display overactivated ROCK.
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