Vascular Smooth Muscle Cell Proliferation Mechanisms

Vascular smooth muscle cells (VSMCs) line the arterial wall and normally maintain a quiescent, contractile phenotype. In response to injury, metabolic stress or inflammatory stimuli, they undergo phenotypic switching to a synthetic state characterised by increased proliferation, migration and extracellular matrix production. Central to this process are mitogenic growth factors such as platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-β (TGF-β), which activate intracellular cascades including ERK/MAPK, PI3K-AKT and RhoA/ROCK pathways. These signals converge on cell cycle regulators such as cyclin D1 and cyclin-dependent kinases, driving G1–S transition. Transcription factors, notably members of the Krüppel-like factor family (KLF4, KLF5), integrate upstream cues to modulate gene networks governing proliferation, differentiation and apoptosis. MicroRNAs add a further layer of post-transcriptional control, fine-tuning expression of key effectors. Epigenetic and post-translational modifications of histones and non-histone proteins also shape VSMC behaviour. Dysregulated VSMC proliferation underlies atherosclerosis, restenosis and hypertension, making these mechanisms attractive targets for novel therapeutics aimed at stabilising plaques, preventing vessel occlusion and restoring vascular homeostasis.

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Vascular Smooth Muscle Cell Proliferation Mechanisms publication trend

The graph below shows the total number of articles in vascular smooth muscle cell proliferation mechanisms across all publications each year (not limited to Nature Index journals).

Technical terms

Phenotypic switching: Transition of VSMCs from a quiescent contractile state to a proliferative synthetic state characterised by altered gene expression and increased matrix synthesis.

PDGF-BB: Platelet-derived growth factor-BB, a dimeric ligand that binds PDGF receptors on VSMCs to initiate proliferative and migratory signalling.

MicroRNA: Small non-coding RNA molecules that regulate gene expression post-transcriptionally by targeting mRNA for degradation or translational repression.

PI3K-AKT pathway: Intracellular signalling cascade activated by growth factors, promoting cell survival and proliferation via phosphorylation of downstream effectors.

Single-cell transcriptomics: High-resolution sequencing technique that measures gene expression in individual cells, revealing cellular heterogeneity within complex tissues.

References

1. Research progress on post-translational modification of proteins and cardiovascular diseases. Cell Death Discovery (2023).
2. Salvianolic Acid B Alleviates High Glucose‐Induced Vascular Smooth Muscle Cell Inflammation by Upregulating the miR‐486a‐5p Expression. Mediators of Inflammation (2024).
3. Deciphering smooth muscle cell heterogeneity in atherosclerotic plaques and constructing model: a multi-omics approach with focus on KLF15/IGFBP4 axis. BMC Genomics (2024).
4. Current knowledge of Krüppel-like factor 5 and vascular remodeling: providing insights for therapeutic strategies. Journal of Molecular Cell Biology (2021).