Smooth Muscle Cells in Vascular Disease
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 20 September 2025 | Viewed by 1244
Special Issue Editor
Interests: atherosclerosis; vascular smooth muscle cell; inflammation; endothelium; cell senescence; apoptosis; lipid metabolism; oxidative stress; nitric oxide; exosomes; vascular calcification; cytokines; growth factors
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Special Issue Information
Dear Colleagues,
Vascular smooth muscle cells (SMCs) are the major constituents of medium- and large-sized arteries. They are arranged in a helical pattern around the vessel lumen and play a key role in controlling blood pressure and blood distribution, as well as maintaining vascular structural integrity. In addition to their physiological properties, SMCs have also been strongly implicated in the pathogenesis of vascular diseases, particularly atherosclerosis, aortic aneurysm and pulmonary hypertension. Unlike adult skeletal or cardiac muscle, which are terminally differentiated, adult SMCs retain remarkable plasticity and can undergo profound and reversible changes in phenotype in response to stimuli or inputs from the environment. In normal healthy arteries, SMCs adopt a quiescent, contractile phenotype characterized by an elongated spindle-shaped morphology and express a unique repertoire of proteins and signaling molecules required for their contractile function. Upon vascular injury, aging or disease states, contractile SMCs can switch to a less differentiated state, characterized by a reduced expression of contractile proteins, and can acquire alternative phenotypes, transforming into foam cells, inflammatory-like cells, mesenchymal stem cells and osteochondrogenic cells, which can contribute both positively and negatively to disease progression. The molecular regulation of SMC behavior involves transcriptional factors, microRNAs and their target genes, epigenetic modifications and numerous environmental cues including growth factor/cytokines, cell–cell contact, extracellular matrix interactions, mechanical force and noxious stimuli. SMC senescence has been also associated with atherosclerosis development. Similar to other cell types, senescent SMCs display defective proliferative potential, increased levels of senescence markers and enhanced cell death. Moreover, senescent SMCs exhibit a more synthetic phenotype and an abnormal response to the vasoactive and regulating peptides produced in the vascular endothelium.
This Special Issue on “Smooth Muscle Cells in Vascular Disease” welcomes original research articles and reviews in the field, with a focus on (but not limited to) the molecular mechanisms that regulate the phenotypic plasticity of SMCs, their potential for monoclonal or oligoclonal expansion, the aberrant interplay between endothelial cells (ECs) and SMCs and the dysregulated signaling pathways activated within the SMCs that contribute to the onset and progression of vascular diseases. I also encourage submissions that aim to define new perspectives and therapeutic strategies targeting SMC-related pathways to clinically treat vascular remodeling and its complications.
Dr. Ida Daniela Perrotta
Guest Editor
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Keywords
- smooth muscle cells (SMCs)
- atherosclerosis
- hypertension
- aortic aneurysm
- vascular ageing
- extracellular matrix
- endothelial cells (ECs)
- SMC senescence
- interleukin
- platelet-derived growth factor
- phenotype switching
- SMC plasticity
- SMC-derived cells
- molecular subtypes
- intimal thickening
- plaque stability
- transcription factors
- microRNAs
- clonality
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