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Title:
An update on the phenotypic switching of vascular smooth muscle cells in the pathogenesis of atherosclerosis | Cellular and Molecular Life Sciences
Description:
Vascular smooth muscle cells (VSMCs) are involved in phenotypic switching in atherosclerosis. This switching is characterized by VSMC dedifferentiation, migration, and transdifferentiation into other cell types. VSMC phenotypic transitions have historically been considered bidirectional processes. Cells can adopt a physiological contraction phenotype or an alternative "synthetic" phenotype in response to injury. However, recent studies, including lineage tracing and single-cell sequencing studies, have shown that VSMCs downregulate contraction markers during atherosclerosis while adopting other phenotypes, including macrophage-like, foam cell, mesenchymal stem-like, myofibroblast-like, and osteochondral-like phenotypes. However, the molecular mechanism and processes regulating the switching of VSMCs at the onset of atherosclerosis are still unclear. This systematic review aims to review the critical outstanding challenges and issues that need further investigation and summarize the current knowledge in this field.
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Keywords {π}
pubmed, google, scholar, cas, smooth, muscle, vascular, cell, cells, central, res, biol, atherosclerosis, zhang, thromb, vasc, phenotypic, arterioscler, wang, circ, calcification, phenotype, differentiation, factor, signaling, expression, article, formation, regulates, switching, long, modulation, nat, circulation, cardiovasc, growth, physiol, gene, human, sci, atherosclerotic, mol, liu, response, disease, zhao, nox, migration, receptor, promotes,
Topics {βοΈ}
wnt3a-mediated rho/rock/jnk signaling pdgf-bb-induced phenotypic modulation platelet-derived mir-223 promotes pdgf-bb-mediated migration activate tgf-beta-smad2/3 signaling carg box-independent manner single-cell rna-seq reveals mir-370/foxo1/cyclin d1 pathway scavenger receptor cxcl16/sr-psox smad3-mediated tgfbeta1 signaling rhoa/rock pathway activation stretch-induced phenotypic modulation month download article/chapter ros-generating nadph oxidases single-cell rna-seq long noncoding rna-gas5 alpha-smooth muscle actin inorganic phosphorus-induced mineralization injury-induced neointimal formation single-cell genomics reveals fibroblast growth factor bridging jagged1-notch3 signaling nox4-based nadph oxidase collagen isotype-specific modulation jak-2/stat-3/cytosolic phospholipase collagen i-dependent functions pi3k/akt signaling pathway klf4-dependent phenotypic modulation rabbit ec-sod gene single-cell sequencing studies redox-sensitive signaling pathways smooth muscle cell vascular smooth muscle hypertension-induced vascular remodeling phenotypic switching induced smooth muscle differentiation smooth muscle cells 5-aza-2β-deoxycytidine smooth muscle actin jak/stat signaling smooth muscle migration srf-dependent transcription low shear stress mesenchymal stem serum response factor promotes vascular homeostasis circular rna enriched histone deacetylases regulate serum responsive factor apolipoprotein e-deficient mice
Questions {β}
- Wissler RW (1967) The arterial medial cell, smooth muscle, or multifunctional mesenchyme?
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headline:An update on the phenotypic switching of vascular smooth muscle cells in the pathogenesis of atherosclerosis
description:Vascular smooth muscle cells (VSMCs) are involved in phenotypic switching in atherosclerosis. This switching is characterized by VSMC dedifferentiation, migration, and transdifferentiation into other cell types. VSMC phenotypic transitions have historically been considered bidirectional processes. Cells can adopt a physiological contraction phenotype or an alternative "synthetic" phenotype in response to injury. However, recent studies, including lineage tracing and single-cell sequencing studies, have shown that VSMCs downregulate contraction markers during atherosclerosis while adopting other phenotypes, including macrophage-like, foam cell, mesenchymal stem-like, myofibroblast-like, and osteochondral-like phenotypes. However, the molecular mechanism and processes regulating the switching of VSMCs at the onset of atherosclerosis are still unclear. This systematic review aims to review the critical outstanding challenges and issues that need further investigation and summarize the current knowledge in this field.
datePublished:2021-12-22T00:00:00Z
dateModified:2021-12-22T00:00:00Z
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VSMCs
Phenotypic switching
Atherosclerosis
Cell Biology
Biomedicine
general
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Biochemistry
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description:Vascular smooth muscle cells (VSMCs) are involved in phenotypic switching in atherosclerosis. This switching is characterized by VSMC dedifferentiation, migration, and transdifferentiation into other cell types. VSMC phenotypic transitions have historically been considered bidirectional processes. Cells can adopt a physiological contraction phenotype or an alternative "synthetic" phenotype in response to injury. However, recent studies, including lineage tracing and single-cell sequencing studies, have shown that VSMCs downregulate contraction markers during atherosclerosis while adopting other phenotypes, including macrophage-like, foam cell, mesenchymal stem-like, myofibroblast-like, and osteochondral-like phenotypes. However, the molecular mechanism and processes regulating the switching of VSMCs at the onset of atherosclerosis are still unclear. This systematic review aims to review the critical outstanding challenges and issues that need further investigation and summarize the current knowledge in this field.
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Atherosclerosis
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general
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