ArticleBioMed research international2017
Serum Amyloid A Induces a Vascular Smooth Muscle Cell Phenotype Switch through the p38 MAPK Signaling Pathway.
Article in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Serum amyloid A and risks of all-cause and cardiovascular mortality in chronic kidney disease: a systematic review and dose-response meta-analysis.Renal failure · 2023Pooled it
- Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026Review
- Serum Amyloid A (SAA) and Its Interaction with High-Density Lipoprotein Cholesterol (HDL-C): A Comprehensive Review.International journal of molecular sciences · 2025Review
- Serum amyloid A: multifaceted roles in inflammation and cellular interactions.Immunologic research · 2025Review
- Luteolin Protects against Vascular Calcification by Modulating SIRT1/CXCR4 Signaling Pathway and Promoting Autophagy.The AAPS journal · 2024Article
- Cyclic Nitroxide 4-Methoxy-Tempo May Decrease Serum Amyloid A-Mediated Renal Fibrosis and Reorganise Collagen Networks in Aortic Plaque.International journal of molecular sciences · 2024Article
- Macrophages as determinants and regulators of systemic sclerosis-related interstitial lung disease.Journal of translational medicine · 2024Article
- Serum amyloid A and metabolic disease: evidence for a critical role in chronic inflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
- 3-Arylcoumarin inhibits vascular calcification by inhibiting the generation of AGEs and anti-oxidative stress.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Expression of airway smooth muscle contractile proteins in children with acute interstitial pneumonia.International journal of experimental pathology · 2022Article
- JIB-04, a histone demethylase Jumonji C domain inhibitor, regulates phenotypic switching of vascular smooth muscle cells.Clinical epigenetics · 2022Article
- High-content analysis of microRNAs involved in the phenotype regulation of vascular smooth muscle cells.Scientific reports · 2022Article
- Extracellular Vesicles From LPS-Treated Macrophages Aggravate Smooth Muscle Cell Calcification by Propagating Inflammation and Oxidative Stress.Frontiers in cell and developmental biology · 2022Article
- A functional role for Serum Amyloid A in the molecular regulation of autophagy in breast cancer.Frontiers in oncology · 2022Article
- SMC-Derived Hyaluronan Modulates Vascular SMC Phenotype in Murine Atherosclerosis.Circulation research · 2021Article
- Adipokines and Arterial Stiffness in Obesity.Medicina (Kaunas, Lithuania) · 2021Review
- Marked Increased Production of Acute Phase Reactants by Skeletal Muscle during Cancer Cachexia.Cancers · 2020Article
- Amyloid Proteins and Peripheral Neuropathy.Cells · 2020Review
- Molecular and Cellular Mechanisms that Induce Arterial Calcification by Indoxyl Sulfate and P-Cresyl Sulfate.Toxins · 2020Review
- Regenerative Therapies for Spinal Cord Injury.Tissue engineering. Part B, Reviews · 2019Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is an important pathological condition which is accompanied by a vascular smooth muscle cell (VSMC) phenotype switch toward a synthetic phenotype. As an acute-phase protein, Serum Amyloid A (SAA) is thought to have a close relationship to atherosclerosis development. However, no study has investigated the direct effect of SAA on the VSMC phenotype switch, as well as the underlying mechanisms. The purpose of our study was to explore the effect of SAA on the VSMC phenotype switch and the potential mechanisms involved. In our study, we found that SAA induced the VSMC phenotype switch which reduced expression of the smooth muscle cell (SMC) marker and enhanced expression of the matrix synthesis related marker. The proliferative ability of VSMCs was also increased by SAA treatment. Furthermore, our research found that SAA activated the ERK1/2 and p38 MAPK signaling pathways. Finally, by applying the ERK1/2 and p38 inhibitors, U0126 and SB203580, we demonstrated that the SAA-induced VSMC phenotype switch was p38-dependent. Taken together, these results indicated that SAA may play an important role in promoting the VSMC phenotype switch through the p38 MAPK signaling pathway.
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