ArticleInternational journal of molecular sciences2022
Targeting the Crosstalk of Immune Response and Vascular Smooth Muscle Cells Phenotype Switch for Arteriovenous Fistula Maturation.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Article
- Vascular Smooth Muscle Cell Metabolic Reprogramming in Arteriovenous Fistula Failure.Biomedicines · 2025Review
- Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025Review
- Vascular Smooth Muscle-Secreted Exosomal X26nt Impedes Atherosclerosis Progression via the c-FOS/XBP1/SOD1 Axis.Immunity, inflammation and disease · 2025Article
- Insights From m6A RNA Methylation: Biomarkers for Diagnosis of Acute Myocardial Infarction.Journal of inflammation research · 2025Article
- Phenotypic switching of vascular smooth muscle cells: a central mechanism in vein graft intimal hyperplasia.Frontiers in cardiovascular medicine · 2025Review
- Review
- Review
- The Pathological Mechanisms and Therapeutic Molecular Targets in Arteriovenous Fistula Dysfunction.International journal of molecular sciences · 2024Review
- Novel Factors Regulating Proliferation, Migration, and Differentiation of Fibroblasts, Keratinocytes, and Vascular Smooth Muscle Cells during Wound Healing.Biomedicines · 2024Review
- Vascular and Perivascular Role in the Regulation of Angiogenesis: Impact on Arteriovenous Fistula Maturation.Archives of internal medicine research · 2024Article
- Therapeutic Potential of Targeting p27Archives of internal medicine research · 2024Article
- Ficolin-2 amplifies inflammation in macrophage-smooth muscle cell cross-talk and increases monocyte transmigration by mechanisms involving IL-1β and IL-6.Scientific reports · 2023Article
- Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023Review
- Oxidized Low-density Lipoproteins and Lipopolysaccharides Augment Carotid Artery Plaque Vulnerability in Hypercholesterolemic Microswine.Cardiology and cardiovascular medicine · 2023Article
- Oncostatin M, Serpins, and Oxidative Stress in Extracellular Matrix Remodeling and Arteriovenous Fistula Maturation.Cardiology and cardiovascular medicine · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Plaque formation, thrombosis, and embolism are the underlying causes of acute cardiovascular events such as myocardial infarction and stroke while early thrombosis and stenosis are common pathologies for the maturation failure of arteriovenous fistula (AVF). Chronic inflammation is a common underlying pathogenesis mediated by innate and adaptive immune response involving infiltration of immune cells and secretion of pro- and anti-inflammatory cytokines. Impaired immune cell infiltration and change in vascular smooth muscle cell (VSMC) phenotype play a crucial role in the underlying pathophysiology. However, the change in the phenotype of VSMCs in a microenvironment of immune cell infiltration and increased secretion of cytokines have not been investigated. Since change in VSMC phenotype regulates vessel remodeling after intimal injury, in this study, we investigated the effect of macrophages and pro-inflammatory cytokines, IL-6, IL-1β, and TNF-α, on the change in VSMC phenotype under in vitro conditions. We also investigated the expression of the markers of VSMC phenotypes in arteries with atherosclerotic plaques and VSMCs isolated from control arteries. We found that the inhibition of cytokine downstream signaling may mitigate the effect of cytokines on the change in VSMCs phenotype. The results of this study support that regulating or targeting immune cell infiltration and function might be a therapeutic strategy to mitigate the effects of chronic inflammation to attenuate plaque formation, early thrombosis, and stenosis, and thus enhance AVF maturation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.