1.Bioresorbable Scaffolds in Coronary Intervention: Unmet Needs and Evolution
Korean Circulation Journal 2018;48(1):24-35
Bioresorbable scaffolds (BRS) represent a novel paradigm in the 40-year history of interventional cardiology. Restoration of cyclic pulsatility and physiologic vasomotion, adaptive vascular remodeling, plaque regression, and removal of the trigger for late adverse events are expected BRS benefits over current metallic drug-eluting stents. However, first-generation BRS devices have significant manufacturing limitations and rely on optimal implantation technique to avoid experiencing an excess of clinical events. There are currently at least 22 BRS devices in different stages of development, including many trials of device iterations with thinner (<150 µm) struts than first-generation BRS. This article reviews the outcomes of commercially available and potentially upcoming BRS, focusing on the most recent stages of clinical development and future directions for each scaffold type.
Angioplasty
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Cardiology
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Drug-Eluting Stents
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Vascular Remodeling
3.Internal relationship between Hippo pathway and pulmonary hypertension
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery 2021;28(11):1376-1380
Pulmonary hypertension is a kind of progressive pulmonary vascular diseases in which there is excessive vasoconstriction and abnormal pulmonary vascular remodeling, and then a gradual increase in pulmonary arterial pressure, and it eventually leads to right ventricular failure and even death. The pathogenesis of pulmonary hypertension is still uncertain, but some studies suggest that Hippo pathway or some components of the Hippo pathway may be involved in the progress of pulmonary hypertension. In this review, we describe the mechanism of the Hippo pathway or some components of the Hippo pathway in the progress of pulmonary hypertension.
Pulmonary hypertension
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Hippo pathway
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pulmonary vascular remodeling
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review
4.New insights into vascular mechanobiology: roles of matrix mechanics in regulating smooth muscle cell function.
Jin WANG ; Juan-Juan ZHU ; Jing ZHOU
Acta Physiologica Sinica 2021;73(2):160-174
Vascular smooth muscle cell (vSMC) is the predominant cell type in the blood vessel wall and is constantly subjected to a complex extracellular microenvironment. Mechanical forces that are conveyed by changes in stiffness/elasticity, geometry and topology of the extracellular matrix have been indicated by experimental studies to affect the phenotype and function of vSMCs. vSMCs perceive the mechanical stimuli from matrix via specialized mechanosensors, translate these stimuli into biochemical signals controlling gene expression and activation, with the consequent modulation in controlling various aspects of SMC behaviors. Changes in vSMC behaviors may further cause disruption of vascular homeostasis and then lead to vascular remodeling. A better understanding of how SMC senses and transduces mechanical forces and how the extracellular mechano-microenvironments regulate SMC phenotype and function may contribute to the development of new therapeutics for vascular diseases.
Biophysics
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Cells, Cultured
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Extracellular Matrix
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Humans
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Muscle, Smooth, Vascular
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Myocytes, Smooth Muscle
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Phenotype
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Vascular Remodeling
5.Vessel Remodeling after Intima-to-Intima Contact Anastomosis.
Hyeonjung YEO ; Hyodong KIM ; Daegu SON ; Changbae HONG ; Sun Young KWON
Archives of Plastic Surgery 2017;44(2):95-100
BACKGROUND: Intima-to-intima microanastomotic vascular remodeling was explored, utilizing a polylactide-caprolactone absorbable vein coupler model (PAVCM), which was designed to simulate a non-absorbable counterpart system with the sole exception of being absorbable. METHODS: Six New Zealand white rabbits were used. After transection of the jugular vein, 2 PAVCMs were placed, 1 at each transected end. The stumps were slipped through the PAVCMs, and the venous wall was everted 90° to achieve intima-to-intima contact. Reanastomosis of the transected jugular vein was performed bilaterally in 3 rabbits. In the other 3 rabbits, the jugular vein (20 mm) harvested from one side was interpositionally grafted to the jugular vein on the opposite side to ease the anastomotic tension. Patency testing, ultrasonography, and histologic assessments were conducted postoperatively at weeks 2, 4, 12, 16, 22, and 26. RESULTS: All anastomotic sites were patent, without stenosis, occlusion, or dilatation. In the histologic sections, immature endothelial regeneration was observed at week 2, which was completed by week 4. Regeneration of the tunica media was noted at week 12. Between week 22 and week 26, the tunica media fully regenerated and the coupler dissipated entirely. CONCLUSIONS: Despite the absence of a coupler to act as an anastomotic buttress, the structure and function of all the vessels appeared normal, even histologically. These outcomes are true milestones in the development of an absorbable vein coupler.
Anastomosis, Surgical
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Constriction, Pathologic
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Dilatation
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Jugular Veins
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Microsurgery
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Rabbits
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Regeneration
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Transplants
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Tunica Media
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Ultrasonography
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Vascular Remodeling
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Vascular Surgical Procedures
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Veins
6.Effect and mechanism of vascular endothelial growth factor-A on pulmonary vascular remodeling in neonatal rats with hypoxic pulmonary hypertension.
Jing CAO ; Jia-Yuan LUO ; Dian WU ; Qian ZHAO ; Ming-Xia LI
Chinese Journal of Contemporary Pediatrics 2021;23(1):103-110
OBJECTIVE:
To study the role of vascular endothelial growth factor-A (VEGF-A) in pulmonary vascular remodeling in neonatal rats with hypoxic pulmonary hypertension (HPH) by regulating survivin (SVV).
METHODS:
A total of 96 neonatal rats were randomly divided into three groups: HPH+VEGF-A group, HPH group, and control group. Each group was further randomly divided into 3-, 7-, 10-, and 14-day subgroups (
RESULTS:
The HPH group had a significantly higher mean RVSP than the control and HPH+VEGF-A groups at each time point (
CONCLUSIONS
Prophylactic intratracheal administration of exogenous VEGF-A in neonatal rats with HPH can inhibit pulmonary vascular remodeling and reduce pulmonary arterial pressure by upregulating the expression of SVV in the early stage of hypoxia. This provides a basis for the interventional treatment of pulmonary vascular remodeling in neonatal HPH.
Animals
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Animals, Newborn
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Hypertension, Pulmonary/etiology*
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Hypoxia
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Pulmonary Artery
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Rats
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Rats, Wistar
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Vascular Endothelial Growth Factor A
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Vascular Remodeling
7.Roles of smooth muscle 22α in vascular homeostasis and vascular remodeling.
Ning ZHANG ; Yong-Qing DOU ; Mei HAN
Acta Physiologica Sinica 2021;73(1):82-88
The research on the molecular mechanism of vascular injury has been a hot topic in recent years since the mechanism can be targeted for the treatment of vascular injury diseases. A large number of studies have found that vascular injury, repair and pathological remodeling are closely related to phenotype switching, abnormal proliferation and migration, and apoptosis of vascular smooth muscle cells (VSMCs). Smooth muscle 22α (SM22α) is a shape change and transformation sensitive F-actin-binding protein. SM22α decorates the contractile filament bundles within cultured VSMCs exhibiting differentiated phenotypes. In addition, SM22α is involved in regulation of cell signaling pathways related to vascular homeostasis and vascular remodeling. Here, we reviewed the recent research progress of SM22α in vascular homeostasis and remodeling.
Cell Proliferation
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Cells, Cultured
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Homeostasis
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Humans
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Muscle Proteins
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Muscle, Smooth, Vascular
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Myocytes, Smooth Muscle
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Phenotype
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Vascular Remodeling
8.Targeting angiogenesis and vascular remodeling as a novel therapeutic approach to liver fibrosis.
Xun-xun WU ; Cai-zhen ZHANG ; Xin WANG ; Yong DIAO
Acta Pharmaceutica Sinica 2015;50(5):535-540
Development of liver fibrosis is closely associated with angiogenesis and abnormal vascular remodeling. Recent studies have highlighted the importance of angiogenesis and vascular remodeling in fibrogenesis, the results that inhibition of angiogenesis is effective in suppression of liver fibrosis demonstrate that therapies with several molecular targets against angiogenesis, inflammation and fibrosis might be beneficial for the treatment of cirrhosis. However, there is some evidence that inhibition of angiogenesis can even worsen fibrosis. This article outlines recent advances regarding the interplay between inflammation, angiogenesis and fibrogenesis in terms of cellular and molecular mechanisms, and suggests a requirement of greater understanding to intervene in these key processes, such as liver sinusoidal endothelial cell fenestration and impact distinct chemokine actions driving monocyte migration and differentiation, for therapeutic benefit in the future.
Humans
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Inflammation
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therapy
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Liver Cirrhosis
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therapy
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Neovascularization, Pathologic
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therapy
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Vascular Remodeling
9.Molecular mechanism of vascular remodeling in hypertension and Chinese medicine intervention.
Chan-Juan ZHANG ; Ya-Ning SHI ; Duan-Fang LIAO ; Ke DU ; Li QIN
Acta Physiologica Sinica 2019;71(2):235-247
Vascular remodeling is a significant pathological characteristic of hypertension, which is regulated by complex regulatory networks. The vascular remodeling may be adaptive initially, however it becomes maladaptive and decompensation eventually and further compromises target organ function, leading to hypertensive cardiovascular complications. This review focuses on the role and mechanisms of vascular remodeling in the pathogenesis and progression of hypertension and its complications. Moreover, the strategies of syndrome differentiation of traditional Chinese medicine application provide clinical and theoretical evidences for hypertensive vascular remodeling therapy. A better understanding of underlying signaling pathways, therapeutic targets in vascular remodeling, as well as screening of active ingredients from traditional Chinese medicine may be able to provide some effective approaches for vascular protection in hypertensive diseases.
Humans
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Hypertension
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physiopathology
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therapy
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Medicine, Chinese Traditional
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Signal Transduction
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Vascular Remodeling
10.Vascular Endothelial Growth Factor and Matrix Metalloproteinase-9 in Acute Asthma.
Kang Seo PARK ; Hung Yong JIN ; Eugene CHOI ; Heung Bum LEE ; Yang Keun RHEE ; Yong Chul LEE
Tuberculosis and Respiratory Diseases 2001;51(6):530-539
BACKGROUND: Bronchial asthma is an inflammatory disease of the airways that is associated with airway remodeling. The vascular endothelial growth factor (VEGF) is a potent, multifunctional cytokine that contributes to angiogenesis and inflammation. Matrix metalloproteinase-9 (MMP-9) is a major proteolytic enzyme that induces bronchial remodeling in asthma. However, there is no data available on the possible role of the VEGF or on the potential relationship between the VEGF and MMP-9 in acute asthma. Therefore, the VEGF was studied to determine whether or not it participates in airway inflammation during acute asthma. An additional aim of this study was to determine whether or not the VEGF levels correlated with the MMP-9 levels in the sputum of acute asthma patients. METHODS: Both the VEGF and MMP-9 levels were measured by an enzyme immunoassay and zymographic analysis in the sputum of patients with either stable asthma or with acute asthma. The VEGF and MMP-9 levels were also evaluated during a spontaneous asthma attack. RESULTS: The VEGF levels were significantly higher in the sputum of acute asthmatic patients than in either the stable patients the control subjects. The VEGF levels in the sputum during asthma exacerbation were significantly higher than those on the remission days, and those levels decreased after decreased after asthma therapy. In acute asthmatic patients, the VEGF levels in the sputum correlated with the number of neutrophils and eosinophils. In addition, a significant correlation was established between the VEGF and MMP-9 levels in the sputum. CONCLUSION: These results suggest that VEGF overproduction is associated with airway inflammation during acute asthma and is related to the MMP-9 function.
Airway Remodeling
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Asthma*
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Eosinophils
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Extracellular Matrix
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Humans
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Immunoenzyme Techniques
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Inflammation
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Matrix Metalloproteinase 9*
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Neutrophils
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Sputum
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Vascular Endothelial Growth Factor A*