Multiple layers of vascular smooth muscle cells (vSMCs) are present in blood vessels forming the media of the vessel wall. vSMCs provide a vessel wall structure, enabling it to contract and relax, thus modulating blood flow. They also play a crucial role in the development of vascular diseases, such as atherosclerosis and aortic aneurysm formation. vSMCs display a remarkable high degree of plasticity. At present, the number of different vSMC phenotypes has only partially been characterized. By mapping vSMC phenotypes in detail and identifying triggers for phenotype switching, the relevance of the different phenotypes in vascular disease may be identified. Up until recently, vSMCs were classified as either contractile or dedifferentiated (ie, synthetic). However, single-cell RNA sequencing studies revealed such dedifferentiated arterial vSMCs to be highly diverse. Currently, no consensus exist about the number of vSMC phenotypes. Therefore, we reviewed the data from relevant single-cell RNA sequencing studies, and classified a total of 6 vSMC phenotypes. The central dedifferentiated vSMC type that we classified is the mesenchymal-like phenotype. Mesenchymal-like vSMCs subsequently seem to differentiate into fibroblast-like, macr...Continue Reading
Platelet-derived growth factor regulates actin isoform expression and growth state in cultured rat aortic smooth muscle cells
Suppression of smooth-muscle alpha-actin expression by platelet-derived growth factor in vascular smooth-muscle cells involves Ras and cytosolic phospholipase A2
Structure and mechanical properties of resistance arteries in hypertension: role of adhesion molecules and extracellular matrix determinants
Contribution of adventitial fibroblasts to neointima formation and vascular remodeling: from innocent bystander to active participant
Osteo/chondrocytic transcription factors and their target genes exhibit distinct patterns of expression in human arterial calcification
Abundant progenitor cells in the adventitia contribute to atherosclerosis of vein grafts in ApoE-deficient mice
Induction of vascular smooth muscle alpha-actin gene transcription in transforming growth factor beta1-activated myofibroblasts mediated by dynamic interplay between the Pur repressor proteins and Sp1/Smad coactivators
Conditional deletion of Krüppel-like factor 4 delays downregulation of smooth muscle cell differentiation markers but accelerates neointimal formation following vascular injury.
Kruppel-like factor 4 is required for the expression of vascular smooth muscle cell differentiation marker genes induced by all-trans retinoic acid
A sonic hedgehog signaling domain in the arterial adventitia supports resident Sca1+ smooth muscle progenitor cells.
Sp1-dependent activation of KLF4 is required for PDGF-BB-induced phenotypic modulation of smooth muscle.
Smooth muscle cells give rise to osteochondrogenic precursors and chondrocytes in calcifying arteries.
MicroRNA-145 regulates OCT4, SOX2, and KLF4 and represses pluripotency in human embryonic stem cells
Free cholesterol overloading induced smooth muscle cells death and activated both ER- and mitochondrial-dependent death pathway.
MicroRNA expression in human airway smooth muscle cells: role of miR-25 in regulation of airway smooth muscle phenotype.
The knockout of miR-143 and -145 alters smooth muscle cell maintenance and vascular homeostasis in mice: correlates with human disease.
Cyclosporine up-regulates Krüppel-like factor-4 (KLF4) in vascular smooth muscle cells and drives phenotypic modulation in vivo.
Notch and transforming growth factor-beta (TGFbeta) signaling pathways cooperatively regulate vascular smooth muscle cell differentiation.
ATRA activates and PDGF-BB represses the SM22α promoter through KLF4 binding to, or dissociating from, its cis-DNA elements
Vascular wall-resident CD44+ multipotent stem cells give rise to pericytes and smooth muscle cells and contribute to new vessel maturation.
down-regulation of Kruppel-like factor-4 (KLF4) by microRNA-143/145 is critical for modulation of vascular smooth muscle cell phenotype by transforming growth factor-beta and bone morphogenetic protein 4.
Epigenetic control of smooth muscle cell differentiation and phenotypic switching in vascular development and disease.
Retinoic acid receptor α mediates all-trans-retinoic acid-induced Klf4 gene expression by regulating Klf4 promoter activity in vascular smooth muscle cells.
Kruppel-like factor 4 contributes to high phosphate-induced phenotypic switching of vascular smooth muscle cells into osteogenic cells.
The fibrillin-1 hypomorphic mgR/mgR murine model of Marfan syndrome shows severe elastolysis in all segments of the aorta
Unchaining the beast; insights from structural and evolutionary studies on TGFβ secretion, sequestration, and activation
Identification of a Klf4-dependent upstream repressor region mediating transcriptional regulation of the myocardin gene in human smooth muscle cells
Aneurysm refers to a bulge of the wall or lining of a vessel commonly occurring in the blood vessels at the base of the septum or within the aorta. In the heart, it usually arises from a patch of weakened tissue in a ventricular wall, which swells into a bubble filled with blood. Discover the latest research on cardiac aneurysm here.
An aortic aneurysm is the weakening and bulging of the blood vessel wall in the aorta. This causes dilatation of the aorta, which is usually asymptomatic but carries the risk of rupture and hemorrhage. Find the latest research on aortic aneurysms here.