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How vascular smooth muscle cell phenotype switching contributes to vascular disease
by
Cao, Genmao
, Zhang, Ruijing
, Xuan, Xuezhen
, Jin, Haijiang
, Hu, Jie
, Dong, Honglin
in
Aging
/ Aneurysms
/ Aortic aneurysm
/ Aortic aneurysms
/ Arteriosclerosis
/ Atherosclerosis
/ Atherosclerosis - metabolism
/ Biomedical and Life Sciences
/ Calcification
/ Cell Biology
/ Cell Proliferation
/ Cholesterol
/ Collagen
/ Coronary vessels
/ Cytokines and Growth Factors
/ Cytoskeleton
/ Development and progression
/ Disease
/ DNA binding proteins
/ Extracellular matrix
/ Gene expression
/ Genetic aspects
/ Genetic transcription
/ Genotype & phenotype
/ Growth factors
/ Humans
/ Inflammation
/ Integrins
/ Leukocyte migration
/ Life Sciences
/ Macrophages
/ Mesenchyme
/ Metabolism
/ Muscle contraction
/ Muscle, Smooth, Vascular - physiology
/ Phenotype
/ Phenotype switching
/ Phenotypes
/ Phenotypic plasticity
/ Physiology
/ Protein-Ligand Interactions
/ Receptors
/ Review
/ Smooth muscle
/ Stem cells
/ Transcription factors
/ Vascular aging
/ Vascular diseases
/ Vascular smooth muscle cells
/ Vascular System Injuries - metabolism
/ Veins & arteries
2022
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How vascular smooth muscle cell phenotype switching contributes to vascular disease
by
Cao, Genmao
, Zhang, Ruijing
, Xuan, Xuezhen
, Jin, Haijiang
, Hu, Jie
, Dong, Honglin
in
Aging
/ Aneurysms
/ Aortic aneurysm
/ Aortic aneurysms
/ Arteriosclerosis
/ Atherosclerosis
/ Atherosclerosis - metabolism
/ Biomedical and Life Sciences
/ Calcification
/ Cell Biology
/ Cell Proliferation
/ Cholesterol
/ Collagen
/ Coronary vessels
/ Cytokines and Growth Factors
/ Cytoskeleton
/ Development and progression
/ Disease
/ DNA binding proteins
/ Extracellular matrix
/ Gene expression
/ Genetic aspects
/ Genetic transcription
/ Genotype & phenotype
/ Growth factors
/ Humans
/ Inflammation
/ Integrins
/ Leukocyte migration
/ Life Sciences
/ Macrophages
/ Mesenchyme
/ Metabolism
/ Muscle contraction
/ Muscle, Smooth, Vascular - physiology
/ Phenotype
/ Phenotype switching
/ Phenotypes
/ Phenotypic plasticity
/ Physiology
/ Protein-Ligand Interactions
/ Receptors
/ Review
/ Smooth muscle
/ Stem cells
/ Transcription factors
/ Vascular aging
/ Vascular diseases
/ Vascular smooth muscle cells
/ Vascular System Injuries - metabolism
/ Veins & arteries
2022
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Do you wish to request the book?
How vascular smooth muscle cell phenotype switching contributes to vascular disease
by
Cao, Genmao
, Zhang, Ruijing
, Xuan, Xuezhen
, Jin, Haijiang
, Hu, Jie
, Dong, Honglin
in
Aging
/ Aneurysms
/ Aortic aneurysm
/ Aortic aneurysms
/ Arteriosclerosis
/ Atherosclerosis
/ Atherosclerosis - metabolism
/ Biomedical and Life Sciences
/ Calcification
/ Cell Biology
/ Cell Proliferation
/ Cholesterol
/ Collagen
/ Coronary vessels
/ Cytokines and Growth Factors
/ Cytoskeleton
/ Development and progression
/ Disease
/ DNA binding proteins
/ Extracellular matrix
/ Gene expression
/ Genetic aspects
/ Genetic transcription
/ Genotype & phenotype
/ Growth factors
/ Humans
/ Inflammation
/ Integrins
/ Leukocyte migration
/ Life Sciences
/ Macrophages
/ Mesenchyme
/ Metabolism
/ Muscle contraction
/ Muscle, Smooth, Vascular - physiology
/ Phenotype
/ Phenotype switching
/ Phenotypes
/ Phenotypic plasticity
/ Physiology
/ Protein-Ligand Interactions
/ Receptors
/ Review
/ Smooth muscle
/ Stem cells
/ Transcription factors
/ Vascular aging
/ Vascular diseases
/ Vascular smooth muscle cells
/ Vascular System Injuries - metabolism
/ Veins & arteries
2022
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How vascular smooth muscle cell phenotype switching contributes to vascular disease
Journal Article
How vascular smooth muscle cell phenotype switching contributes to vascular disease
2022
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Overview
Vascular smooth muscle cells (VSMCs) are the most abundant cell in vessels. Earlier experiments have found that VSMCs possess high plasticity. Vascular injury stimulates VSMCs to switch into a dedifferentiated type, also known as synthetic VSMCs, with a high migration and proliferation capacity for repairing vascular injury. In recent years, largely owing to rapid technological advances in single-cell sequencing and cell-lineage tracing techniques, multiple VSMCs phenotypes have been uncovered in vascular aging, atherosclerosis (AS), aortic aneurysm (AA), etc. These VSMCs all down-regulate contractile proteins such as α-SMA and calponin1, and obtain specific markers and similar cellular functions of osteoblast, fibroblast, macrophage, and mesenchymal cells. This highly plastic phenotype transformation is regulated by a complex network consisting of circulating plasma substances, transcription factors, growth factors, inflammatory factors, non-coding RNAs, integrin family, and Notch pathway. This review focuses on phenotypic characteristics, molecular profile and the functional role of VSMCs phenotype landscape; the molecular mechanism regulating VSMCs phenotype switching; and the contribution of VSMCs phenotype switching to vascular aging, AS, and AA.
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Video Abstract
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
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