GO:1905176 positive regulation of vascular associated smooth muscle cell dedifferentiation: Phenotypic Switching, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1905176 describes any process that activates or increases the frequency, rate or extent of vascular smooth muscle cell (VSMC) dedifferentiation, the transition from a quiescent contractile phenotype to a synthetic, proliferative, migratory state.
• VSMC dedifferentiation is driven by downregulation of contractile markers such as ACTA2, MYH11, LMOD1, SYNPO2, PDLIM7, PLN and SYNM, and is a hallmark of atherosclerosis, restenosis and neointimal hyperplasia [1,6].
• Positive regulators of VSMC dedifferentiation include inflammatory cytokines such as IL-1beta and PGE2, which amplify phenotypic modulation through adenylyl cyclase 8 and EP3 receptor signaling.
• Negative regulators that restrain dedifferentiation include TFEB, which ameliorates arterial smooth muscle cell dedifferentiation and neointima formation in high-fat-diet mice, and La ribonucleoprotein 7 (LARP7), which protects the contractile phenotype in chronic kidney disease.
• The COP9 signalosome deneddylation activity is required for VSMC proliferation but not for dedifferentiation in neointimal hyperplasia, showing that proliferation and dedifferentiation are genetically separable processes.
• CRISPR knockout, point-mutation, knock-in and overexpression models are essential to establish causality for candidate genes that positively regulate VSMC dedifferentiation [2,5,8].
Description
GO:1905176, positive regulation of vascular associated smooth muscle cell dedifferentiation, is a Gene Ontology biological process term that captures any molecular event that activates or increases the frequency, rate or extent of the loss of the contractile phenotype in vascular smooth muscle cells (VSMCs). In the mature vessel wall, VSMCs are normally quiescent and express a repertoire of contractile proteins that maintain vascular tone and structural integrity; dedifferentiation reverses this program and converts cells into a synthetic, proliferative and migratory state [1,6]. This phenotypic switching is not a passive loss of markers but an actively regulated process, and GO:1905176 specifically annotates the positive regulatory inputs that drive it [1,7]. Researchers study GO:1905176 because it sits at the causal center of occlusive vascular disease. In atherosclerosis, phenotypic modulation of VSMCs is associated with coordinated downregulation of LMOD1, SYNPO2, PDLIM7, PLN and SYNM, and this signature correlates with plaque progression. In neointimal hyperplasia after vascular injury, VSMC dedifferentiation precedes and accompanies lesion formation, and interventions that block dedifferentiation, such as TFEB activation, reduce neointima formation in mice with high-fat diet. The term therefore provides a controlled vocabulary for linking molecular perturbations to a defined cellular outcome, which is essential for reproducible vascular biology research [1,5,8]. Because GO:1905176 is a regulation term rather than a single pathway, its annotation space spans cytokines, transcription factors, epigenetic regulators, calcium channels and proteostasis machinery [2,3,5,7,8]. This breadth makes it a useful integration node for multi-omic studies and for CRISPR-based causal screens, but it also means that any claim about positive regulation must be tied to a specific molecular perturbation and a validated dedifferentiation readout [2,5,8].
positive regulation of vascular associated smooth muscle cell dedifferentiation At A Glance
| GO ID | GO:1905176 |
|---|---|
| GO term | positive regulation of vascular associated smooth muscle cell dedifferentiation |
| Ontology | biological_process |
| Synonym | activation of vascular smooth muscle cell dedifferentiation; positive regulation of vascular smooth muscle cell dedifferentiation; up regulation of vascular smooth muscle cell dedifferentiation; up-regulation of vascular smooth muscle cell dedifferentiation; upregulation of vascular smooth muscle cell dedifferentiation |
| Major function | Increases the frequency, rate or extent of the transition from a contractile to a synthetic VSMC phenotype [1,6] |
| Biological context | Atherosclerosis, neointimal hyperplasia, restenosis, chronic kidney disease-associated vascular remodeling [2,5,6,8] |
| Representative positive regulators | IL-1beta and PGE2 signaling via adenylyl cyclase 8 |
| Representative negative regulators | TFEB, LARP7, cytoglobin |
| Key contractile markers lost | ACTA2, MYH11, LMOD1, SYNPO2, PDLIM7, PLN, SYNM [1,6] |
What Is GO:1905176?
GO:1905176 is defined by QuickGO as any process that activates or increases the frequency, rate or extent of vascular smooth muscle cell dedifferentiation. In practical terms, it is the positive-regulatory arm of VSMC phenotypic switching: it does not describe the dedifferentiated state itself, but the upstream or concurrent events that promote the transition away from the contractile program [1,6]. A gene or chemical is annotated to GO:1905176 when experimental evidence shows that its gain of function or activation increases dedifferentiation, typically measured by reduced contractile marker expression, increased synthetic markers, or enhanced proliferation and migration of VSMCs [1,5,7].
Why Is positive regulation of vascular associated smooth muscle cell dedifferentiation Important in Cell Biology?
GO:1905176 matters because VSMC dedifferentiation is a reversible, druggable node in the pathogenesis of the most common occlusive vascular diseases. Unlike cell death, dedifferentiation can in principle be halted or reversed, and published work shows that restoring contractile regulators such as TFEB reduces neointima formation in vivo. At the same time, the term is mechanistically precise enough to separate dedifferentiation from proliferation: COP9 signalosome deneddylation activity is required for VSMC proliferation but not for dedifferentiation in neointimal hyperplasia, demonstrating that the two processes can be uncoupled genetically. This distinction is critical for target selection, because an intervention that only blocks proliferation may leave the dedifferentiated, matrix-secreting phenotype intact. Finally, GO:1905176 provides a shared annotation framework that allows CRISPR screens, transcriptomic signatures and histopathological observations to be compared across laboratories [1,6].
• VSMC dedifferentiation is a defining feature of atherosclerotic plaque progression and is associated with downregulation of LMOD1, SYNPO2, PDLIM7, PLN and SYNM.
• Positive regulation of dedifferentiation contributes to neointimal hyperplasia after vascular injury, a major cause of restenosis [5,8].
• Inflammatory mediators such as IL-1beta and PGE2 amplify VSMC de-differentiation through EP3 receptor and adenylyl cyclase 8 signaling, linking inflammation to phenotypic switching.
• Negative regulators such as TFEB and LARP7 protect the contractile phenotype, defining candidate therapeutic targets [2,5].
• Cytoglobin acts as a negative regulator of atherosclerotic fibrous cap development, indicating that oxygen-handling proteins modulate VSMC phenotype in plaques.
• Calcium channel regulation intersects with VSMC phenotype and is modulated by statins and calcium channel blockers, connecting GO:1905176 to cardiovascular pharmacology.
• The process is genetically separable from proliferation, as shown by COP9 signalosome deneddylation mutants.
• Contractile gene expression is coordinately regulated at the transcriptional level, making the term amenable to transcriptomic and epigenomic dissection.
• CRISPR-based causal screens can identify positive regulators of dedifferentiation in an unbiased manner [2,5,8].
• GO:1905176 supports reproducible annotation of vascular remodeling phenotypes across model systems [1,6].
What Happens During positive regulation of vascular associated smooth muscle cell dedifferentiation?
Initiation by inflammatory and growth-factor signals
In simple terms: Inflammation and growth signals tell the muscle cell to stop being a quiet contractile cell and start behaving like a proliferative, synthetic cell.
Positive regulation of VSMC dedifferentiation is frequently initiated by extracellular cues. IL-1beta, a pro-inflammatory cytokine, promotes VSMC de-differentiation, and PGE2 amplifies this effect through emerging expression of adenylyl cyclase 8 downstream of EP3 receptor signaling. These signals converge on transcriptional programs that repress contractile gene expression, the earliest measurable step of dedifferentiation [1,7]. Because the initiating ligands are well defined, this stage is experimentally tractable with cytokine stimulation and receptor blockade.
Transcriptional repression of the contractile program
In simple terms: The cell turns down the genes that make it a muscle cell.
Dedifferentiation requires coordinated downregulation of smooth muscle cell-specific genes. Expressional regulation of these genes is a central mechanism of phenotypic modulation, and the contractile markers ACTA2, MYH11, LMOD1, SYNPO2, PDLIM7, PLN and SYNM are downregulated in atherosclerotic phenotypic modulation [1,6]. This coordinated repression distinguishes dedifferentiation from nonspecific cell stress and provides a quantitative readout for GO:1905176 activity [1,6].
Epigenetic and proteostatic control of the switch
In simple terms: Helper proteins that package DNA and recycle other proteins decide whether the muscle-cell program stays on or off.
The switch is reinforced by chromatin-associated and proteostatic regulators. LARP7 protects the VSMC contractile phenotype in chronic kidney disease by coupling with P300, indicating that RNA-binding and acetyltransferase complexes restrain dedifferentiation. Conversely, COP9 signalosome deneddylation activity is required for VSMC proliferation but not for dedifferentiation in neointimal hyperplasia, showing that cullin-RING ligase regulation selectively controls the proliferative arm rather than the phenotypic switch itself. These findings argue that positive regulation of dedifferentiation is not simply the inverse of proliferation.
Metabolic and oxygen-sensing modulation
In simple terms: How the cell handles oxygen and energy can push it toward or away from dedifferentiation.
Metabolic regulators influence the phenotypic state. TFEB activation ameliorates dedifferentiation of arterial smooth muscle cells and neointima formation in mice with high-fat diet, linking lysosomal and metabolic transcriptional programs to suppression of dedifferentiation. Cytoglobin, a globin-family oxygen-binding protein, is a negative regulator of atherosclerotic fibrous cap development, implicating oxygen handling in the modulation of VSMC behavior within plaques. These observations place GO:1905176 at the intersection of metabolism, oxygen sensing and vascular remodeling [4,5].
Functional consequences: proliferation, migration and matrix remodeling
In simple terms: Once dedifferentiated, the cell multiplies, moves and rebuilds the vessel wall in a way that can narrow the artery.
The endpoint of positive regulation of VSMC dedifferentiation is a synthetic phenotype characterized by increased proliferative and migratory capacity and altered matrix production [1,6]. In neointimal hyperplasia, this contributes to lesion formation, and interventions that block dedifferentiation reduce neointima in vivo. Because proliferation can be uncoupled from dedifferentiation, assays must measure both phenotypic markers and proliferative indices to correctly assign a gene to GO:1905176.
Key Genes Involved in GO:1905176 positive regulation of vascular associated smooth muscle cell dedifferentiation
The following genes and proteins have been experimentally linked to the regulation of vascular smooth muscle cell dedifferentiation and are the most relevant candidates for functional studies of GO:1905176.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ACTA2 | Contractile marker whose downregulation defines dedifferentiation | Readout of phenotypic switching in atherosclerosis and injury models [1,6] |
| MYH11 | Smooth muscle myosin heavy chain contractile marker | Quantitative marker of contractile phenotype loss |
| LMOD1 | Contractile cytoskeletal regulator | Downregulated in atherosclerotic phenotypic modulation |
| SYNPO2 | Actin-associated contractile protein | Downregulated in atherosclerotic phenotypic modulation |
| PDLIM7 | Cytoskeletal adaptor protein | Downregulated in atherosclerotic phenotypic modulation |
| PLN | Phospholamban, calcium handling regulator | Downregulated in atherosclerotic phenotypic modulation |
| SYNM | Synemin, intermediate filament protein | Downregulated in atherosclerotic phenotypic modulation |
| TFEB | Transcription factor that suppresses dedifferentiation | Activation ameliorates dedifferentiation and neointima formation |
| LARP7 | RNA-binding protein protecting contractile phenotype | Couples with P300 in chronic kidney disease |
| EP300 | Acetyltransferase partner of LARP7 | Epigenetic maintenance of contractile state |
| CYGB | Cytoglobin, oxygen-binding protein | Negative regulator of atherosclerotic fibrous cap development |
| IL1B | Pro-inflammatory cytokine | Promotes VSMC de-differentiation |
| PTGER3 | PGE2 receptor EP3 | Mediates PGE2 amplification of de-differentiation |
| ADCY8 | Adenylyl cyclase 8 | Emerging expression mediates PGE2 effects on de-differentiation |
| COPS5 | COP9 signalosome subunit | Deneddylation required for proliferation but not dedifferentiation |
| CACNA1C | Voltage-gated calcium channel subunit | Calcium channel regulation intersects with VSMC phenotype |
How Is positive regulation of vascular associated smooth muscle cell dedifferentiation Regulated?
GO:1905176 is regulated at multiple levels. Extracellularly, inflammatory cytokines such as IL-1beta and lipid mediators such as PGE2 positively regulate dedifferentiation, with PGE2 acting through EP3 receptor signaling and emerging adenylyl cyclase 8 expression. Intracellularly, transcriptional and epigenetic regulators set the threshold for the switch: LARP7 protects the contractile phenotype by coupling with P300, while TFEB activation suppresses dedifferentiation and neointima formation in high-fat-diet mice. Proteostatic control adds another layer, since COP9 signalosome deneddylation activity is required for VSMC proliferation but not for dedifferentiation, indicating that the regulation of dedifferentiation is genetically separable from proliferative signaling. Calcium channel regulation further modulates VSMC phenotype and is influenced pharmacologically by statins and calcium channel blockers. Together, these inputs define a regulatory network in which positive and negative regulators compete to determine the phenotypic state [2,3,5,7,8].
positive regulation of vascular associated smooth muscle cell dedifferentiation and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| LMOD1 | Atherosclerotic phenotypic modulation | Apoe-/- or Ldlr-/- mice with high-fat diet; human plaque transcriptomics |
| TFEB | Neointima formation and dedifferentiation | High-fat-diet mouse vascular injury model with TFEB activation |
| LARP7 | Chronic kidney disease-associated vascular remodeling | CKD mouse models with VSMC-specific LARP7 knockout |
| CYGB | Atherosclerotic fibrous cap development | Cygb knockout mice crossed to atherosclerosis-prone backgrounds |
| COPS5 | Neointimal hyperplasia and proliferation | Vascular injury models with COP9 signalosome perturbation |
Atherosclerosis and plaque instability
VSMC phenotypic modulation is a hallmark of atherosclerosis, and dedifferentiation is associated with downregulation of LMOD1, SYNPO2, PDLIM7, PLN and SYNM in human plaques. Positive regulation of dedifferentiation contributes to the synthetic VSMC population that accumulates in the intima and influences fibrous cap composition, and cytoglobin has been identified as a negative regulator of atherosclerotic fibrous cap development. Because cap thickness determines plaque stability, genes annotated to GO:1905176 are candidate modifiers of clinical outcomes [4,6].
Neointimal hyperplasia and restenosis
After vascular injury, VSMC dedifferentiation precedes neointimal lesion formation, and interventions that block dedifferentiation reduce neointima in mice with high-fat diet. The COP9 signalosome is required for VSMC proliferation but not for dedifferentiation in neointimal hyperplasia, which means that restenosis can be driven by proliferative signals even when the phenotypic switch is independently regulated. This distinction has direct implications for anti-restenotic target selection.
Chronic kidney disease-associated vascular remodeling
In chronic kidney disease, LARP7 protects the VSMC contractile phenotype by coupling with P300, and loss of this protection would be expected to promote dedifferentiation and vascular remodeling. This links GO:1905176 to uremic vasculopathy and provides a molecular entry point for studying CKD-associated cardiovascular complications.
Inflammation-driven vascular disease
IL-1beta and PGE2 positively regulate VSMC de-differentiation, with PGE2 amplifying IL-1beta effects through EP3 receptor signaling and adenylyl cyclase 8 expression. This places GO:1905176 downstream of innate immune activation and suggests that anti-inflammatory strategies may indirectly modulate phenotypic switching.
From positive regulation of vascular associated smooth muscle cell dedifferentiation-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for VSMC dedifferentiation? | CRISPR knockout in primary VSMC or smooth muscle cell lines with contractile marker readouts [1,6] |
| Does a specific phosphorylation or acetylation site control dedifferentiation? | Point-mutation knock-in at the endogenous locus [2,5] |
| Does a disease-associated variant alter dedifferentiation? | Knock-in of the variant allele followed by phenotypic marker quantification [2,6] |
| Where and when is the protein expressed during phenotypic switching? | Tagged knock-in with immunofluorescence or live imaging [2,5] |
| Does forced expression of a negative regulator block dedifferentiation? | Overexpression of TFEB, LARP7 or cytoglobin in VSMC [2,4,5] |
| Which genes positively regulate dedifferentiation in an unbiased manner? | CRISPR library screening with contractile marker-based selection [2,5,8] |
How to Study the positive regulation of vascular associated smooth muscle cell dedifferentiation Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Global transcriptome including contractile gene module | Signature of VSMC dedifferentiation in vitro and in vivo [1,6] |
| qPCR | Expression of ACTA2, MYH11, LMOD1, SYNPO2, PDLIM7, PLN, SYNM | Rapid readout of phenotypic switching [1,6] |
| Immunofluorescence | Protein localization and contractile marker intensity | Tissue-level confirmation of dedifferentiation [1,5] |
| Immunoblotting | Protein abundance of contractile and synthetic markers | Validation of transcript changes [1,6] |
| EdU incorporation | DNA synthesis and proliferation | Separating proliferation from dedifferentiation |
| Migration assay | Cell motility | Functional consequence of synthetic phenotype |
| Histomorphometry | Neointima and fibrous cap thickness | In vivo disease relevance [4,5] |
| CRISPR library screening | Unbiased identification of regulators | Discovery of positive regulators of dedifferentiation [2,5,8] |
Transcriptomic profiling of contractile and synthetic markers
RNA-seq and targeted qPCR are used to quantify the coordinated downregulation of ACTA2, MYH11, LMOD1, SYNPO2, PDLIM7, PLN and SYNM that defines VSMC dedifferentiation [1,6]. Because these markers change as a module, transcriptomic signatures provide a robust readout for GO:1905176 activity across perturbations [1,6].
Protein-level and imaging assays
Immunofluorescence and immunoblotting for contractile proteins confirm that transcript changes translate into phenotypic remodeling, and co-staining with proliferation markers helps separate dedifferentiation from proliferation [1,5,8]. Tagged knock-in lines enable tracking of candidate regulators during the switch [2,5].
Functional proliferation and migration assays
Because dedifferentiation is genetically separable from proliferation, functional assays such as EdU incorporation, scratch wound migration and transwell migration are used alongside phenotypic markers [5,8]. COP9 signalosome studies specifically demonstrate the value of measuring both arms independently.
In vivo vascular injury and disease models
Mouse models of vascular injury, high-fat-diet feeding and chronic kidney disease provide the physiological context in which positive regulation of dedifferentiation contributes to neointima formation and plaque progression [2,4,5,8]. Histological quantification of neointima and fibrous cap thickness links molecular findings to disease phenotypes [4,5].
How CRISPR Can Be Used to Study GO:1905176 positive regulation of vascular associated smooth muscle cell dedifferentiation
Knockout
CRISPR knockout of candidate positive regulators is used to test whether loss of function reduces VSMC dedifferentiation, measured by preserved contractile marker expression and reduced proliferation or migration [2,5,8]. Knockout of negative regulators such as LARP7 or TFEB targets would be expected to enhance dedifferentiation, providing bidirectional validation of GO:1905176 annotations [2,5].
Point Mutation
Point-mutation knock-in allows precise testing of post-translational regulatory sites, such as acetylation or phosphorylation residues in transcriptional and epigenetic regulators that control the contractile program [2,5]. This approach distinguishes catalytic and non-catalytic functions of enzymes such as acetyltransferases and kinases in phenotypic switching.
Knock-in
Knock-in of reporters, tags or disease-associated variants enables tracking of endogenous regulators during dedifferentiation and tests whether specific alleles alter the phenotypic switch [2,5,6]. Tagged knock-in lines are particularly useful for imaging the dynamic localization of LARP7, TFEB and related factors [2,5].
Overexpression
Overexpression of candidate negative regulators such as TFEB, LARP7 or cytoglobin tests whether forced expression is sufficient to block dedifferentiation and reduce neointima or fibrous cap pathology [2,4,5]. Conversely, overexpression of positive regulators such as components of IL-1beta or PGE2 signaling can drive the synthetic phenotype.
How EDITGENE Supports positive regulation of vascular associated smooth muscle cell dedifferentiation Research
Researchers studying positive regulation of vascular associated smooth muscle cell dedifferentiation-related genes often need to determine whether a candidate gene is causally involved in the phenotypic switch or merely correlated with it. Establishing causality requires controlled genetic perturbation in relevant vascular cell models, combined with quantitative readouts of contractile marker loss and functional phenotypic changes [1,5,8]. EDITGENE provides the full spectrum of CRISPR engineering services needed to build those models.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of vascular associated smooth muscle cell dedifferentiation research.
Frequently Asked Questions About positive regulation of vascular associated smooth muscle cell dedifferentiation
What is GO:1905176?
GO:1905176 is the Gene Ontology biological process term for positive regulation of vascular associated smooth muscle cell dedifferentiation, meaning any process that activates or increases the frequency, rate or extent of VSMC dedifferentiation.
What is vascular smooth muscle cell dedifferentiation?
It is the transition of a quiescent contractile VSMC into a synthetic, proliferative and migratory cell, marked by downregulation of contractile genes such as ACTA2, MYH11, LMOD1, SYNPO2, PDLIM7, PLN and SYNM [1,6].
What genes are involved in positive regulation of vascular smooth muscle cell dedifferentiation?
Reported regulators include IL1B, PTGER3 and ADCY8 as positive inputs, and TFEB, LARP7, EP300 and CYGB as negative regulators that restrain the switch [2,4,5].
How is VSMC dedifferentiation measured?
Common readouts are RNA-seq or qPCR of contractile markers, immunofluorescence and immunoblotting of contractile proteins, and functional proliferation and migration assays [1,5,6,8].
Why is VSMC dedifferentiation important in atherosclerosis?
Phenotypic modulation of VSMCs is associated with downregulation of LMOD1, SYNPO2, PDLIM7, PLN and SYNM in atherosclerosis, and contributes to plaque composition and fibrous cap development [4,6].
Can dedifferentiation be separated from proliferation?
Yes. COP9 signalosome deneddylation activity is required for VSMC proliferation but not for dedifferentiation in neointimal hyperplasia, showing the two processes are genetically separable.
What role does TFEB play in VSMC dedifferentiation?
TFEB activation ameliorates dedifferentiation of arterial smooth muscle cells and neointima formation in mice with high-fat diet.
How does LARP7 affect the VSMC contractile phenotype?
LARP7 protects the VSMC contractile phenotype in chronic kidney disease by coupling with P300.
What experimental models are used to study GO:1905176?
Models include primary VSMC cultures, CRISPR knockout and knock-in lines, vascular injury mouse models, high-fat-diet mice and chronic kidney disease models [2,4,5,8].
How can CRISPR help study positive regulation of VSMC dedifferentiation?
CRISPR knockout, point-mutation, knock-in, overexpression and library screening establish causality and identify novel regulators of the phenotypic switch [2,5,8].
Conclusion
GO:1905176 provides a precise annotation for the positive regulatory inputs that drive vascular smooth muscle cell dedifferentiation, a process central to atherosclerosis, neointimal hyperplasia and chronic kidney disease-associated vascular remodeling [2,4,5,6,8]. The literature shows that this switch is controlled by a balance of inflammatory drivers such as IL-1beta and PGE2 and protective factors such as TFEB, LARP7 and cytoglobin [2,4,5], and that it can be uncoupled from proliferation. Because the phenotype is reversible in principle, genes annotated to GO:1905176 are attractive targets for mechanistic and therapeutic studies [5,8]. Rigorous causal testing with CRISPR-engineered models and quantitative contractile marker readouts will be essential to translate these annotations into vascular disease interventions [1,2,5,8].
References
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- 2. Wu H et al.. 2025. La Ribonucleoprotein 7 Protects Vascular Smooth Muscle Cell Contractile Phenotype in CKD by Coupling with P300.. J Am Soc Nephrol 36(12):2364-2377 PMID: 40522739
- 3. Clunn GF et al.. 2010. Calcium channel regulation in vascular smooth muscle cells: synergistic effects of statins and calcium channel blockers.. Int J Cardiol 139(1):2-6 PMID: 19523699
- 4. Gilliard K et al.. 2026. Smooth Muscle Cell Cytoglobin is a Negative Regulator of Atherosclerotic Fibrous Cap Development.. bioRxiv PMID: 42427674
- 5. Wang YT et al.. 2019. Activation of TFEB ameliorates dedifferentiation of arterial smooth muscle cells and neointima formation in mice with high-fat diet.. Cell Death Dis 10(9):676 PMID: 31515484
- 6. Perisic Matic L et al.. 2016. Phenotypic Modulation of Smooth Muscle Cells in Atherosclerosis Is Associated With Downregulation of LMOD1, SYNPO2, PDLIM7, PLN, and SYNM.. Arterioscler Thromb Vasc Biol 36(9):1947-61 PMID: 27470516
- 7. Clément N et al.. 2006. PGE2 amplifies the effects of IL-1beta on vascular smooth muscle cell de-differentiation: a consequence of the versatility of PGE2 receptors 3 due to the emerging expression of adenylyl cyclase 8.. J Cell Physiol 208(3):495-505 PMID: 16741924
- 8. Giri S et al.. 2026. COP9 signalosome deneddylation activity is required for proliferation but not dedifferentiation of vascular smooth muscle cells in neointimal hyperplasia.. Am J Physiol Heart Circ Physiol 331(1):H130-H141 PMID: 42233540
