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Pathological Mechanisms Involved in Restenosis Progression

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 December 2022) | Viewed by 2791

Special Issue Editor


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Guest Editor
School of Pharmacy, Taipei Medical University, Taipei 110, Taiwan
Interests: restenosis; gene therapy; cancer research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Percutaneous coronary intervention (PCI) has been widely used for acute coronary syndrome (ACS). However, restenosis has always remained to be a major concern for the effectiveness and complication of PCI. Although the development of drug eluting stents (DESs) has significantly reduced the restenosis rate down to 5-20% of patients after PCI as compared to bare metal stents (BMS), intervention or prediction of restenosis still remains to be an important issue to maintain the life quality of patients receiving PCI. Novel DES with even lower restenosis rate or pharmacological approaches to prevent restenosis or identification of precise risk factors leading to restenosis are all awaiting further exploration. This Special Issue "Pathological Mechanisms Involved in Restenosis Progression" will call for papers with outstanding findings to eliminate the incidence of restenosis or to identify biomarkers for the prediction of restenosis.

Prof. Dr. Chieh-Hsi Wu
Guest Editor

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Keywords

  • restenosis
  • angioplasty
  • stent
  • biomarkers
  • intervention
  • pharmacology

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Published Papers (1 paper)

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Research

22 pages, 8617 KiB  
Article
BMPER Improves Vascular Remodeling and the Contractile Vascular SMC Phenotype
by Franziska Pankratz, Aziza Maksudova, Roman Goesele, Lena Meier, Kora Proelss, Katia Marenne, Ann-Kathrin Thut, Gerhard Sengle, Annkatrin Correns, Jeanina Begelspacher, Deniz Alkis, Patrick M. Siegel, Christian Smolka, Sebastian Grundmann, Martin Moser, Qian Zhou and Jennifer S. Esser
Int. J. Mol. Sci. 2023, 24(5), 4950; https://doi.org/10.3390/ijms24054950 - 3 Mar 2023
Cited by 2 | Viewed by 2378
Abstract
Dedifferentiated vascular smooth muscle cells (vSMCs) play an essential role in neointima formation, and we now aim to investigate the role of the bone morphogenetic protein (BMP) modulator BMPER (BMP endothelial cell precursor-derived regulator) in neointima formation. To assess BMPER expression in arterial [...] Read more.
Dedifferentiated vascular smooth muscle cells (vSMCs) play an essential role in neointima formation, and we now aim to investigate the role of the bone morphogenetic protein (BMP) modulator BMPER (BMP endothelial cell precursor-derived regulator) in neointima formation. To assess BMPER expression in arterial restenosis, we used a mouse carotid ligation model with perivascular cuff placement. Overall BMPER expression after vessel injury was increased; however, expression in the tunica media was decreased compared to untreated control. Consistently, BMPER expression was decreased in proliferative, dedifferentiated vSMC in vitro. C57BL/6_Bmper+/− mice displayed increased neointima formation 21 days after carotid ligation and enhanced expression of Col3A1, MMP2, and MMP9. Silencing of BMPER increased the proliferation and migration capacity of primary vSMCs, as well as reduced contractibility and expression of contractile markers, whereas stimulation with recombinant BMPER protein had the opposite effect. Mechanistically, we showed that BMPER binds insulin-like growth factor-binding protein 4 (IGFBP4), resulting in the modulation of IGF signaling. Furthermore, perivascular application of recombinant BMPER protein prevented neointima formation and ECM deposition in C57BL/6N mice after carotid ligation. Our data demonstrate that BMPER stimulation causes a contractile vSMC phenotype and suggest that BMPER has the potential for a future therapeutic agent in occlusive cardiovascular diseases. Full article
(This article belongs to the Special Issue Pathological Mechanisms Involved in Restenosis Progression)
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