Transdifferentiation of Vascular Smooth Muscle Cells to Macrophage-Like Cells During Atherogenesis

Feil, Susanne; Fehrenbacher, Birgit; Łukowski, Robert; Eßmann, Frank; Schulze‐Osthoff, Klaus; Schaller, Martin; Feil, Robert

doi:10.1161/circresaha.115.304634

Cited by 465 publications

(460 citation statements)

References 31 publications

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“…Depending on their local environment, T lymphocytes can be stimulated to secrete proinflammatory T h 1 cytokines such IL-1, IL-6, and TNF; or T h 2 cytokines such as IL-4, IL-10, and IL-13, which promote resolution of inflammation. IL-1 and TNF signalling is primarily mediated by p38 mitogen- [131][132][133] , have produced in vivo data consistent with these phenomena: 30-40% of cells classified as plaque macrophages were of vascular smooth muscle cell origin. It is too early to discern the contribution of these cells to the pathological process during atherogenesis, but at least in cell culture, they do not share the molecular signature or the functional properties of activated macrophages 134 .…”

Section: Atherosclerosis Pathogenesismentioning

confidence: 77%

“…A number of experiments in mice, and notably humans [131][132][133] , have produced in vivo data consistent with these phenomena: 30-40% of cells classified as plaque macrophages were of vascular smooth muscle cell origin. It is too early to discern the contribution of these cells to the pathological process during atherogenesis, but at least in cell culture, they do not share the molecular signature or the functional properties of activated macrophages 134 .…”

Section: Atherosclerosis Pathogenesismentioning

confidence: 80%

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Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Ruparelia¹,

Chai²,

Fisher³

et al. 2017

Nat Rev Cardiol

194

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Inflammatory processes are firmly established as central to the development and complications of cardiovascular diseases. Elevated levels of inflammatory markers have been shown to be predictive of future cardiovascular events. The specific targeting of these processes in experimental models has been shown to attenuate myocardial and arterial injury, reduce disease progression, and promote healing. However, the translation of these observations and the demonstration of clear efficacy in clinical practice have been disappointing. A major limitation might be that tools currently used to measure 'inflammation' are insufficiently precise and do not provide information about disease site, activity, or discriminate between functionally important activation pathways. The challenge, therefore, is to make measures of inflammation that are more meaningful, and which can guide specific targeted therapies. In this Review, we consider the roles of inflammatory processes in the related pathologies of atherosclerosis and acute myocardial infarction (AMI), by providing an evaluation of the known and emerging inflammatory pathways. We highlight contemporary techniques to characterize and quantify inflammation, and consider how they might be used to guide specific treatments. Finally, we discuss emerging opportunities in the field, including current limitations and challenges that are the focus of ongoing study.Inflammation and its failure to resolve are firmly established as central to the development and complications of several cardiovascular diseases [1][2][3] . Elevated levels of markers of inflammation, such as C-reactive protein (CRP) and serum amyloid A (SAA), have been shown to be predictive of future cardiovascular events across a range of clinical settings [4][5][6] . The role of the innate immune system in the pathogenesis of cardiovascular diseases has been an area of particular focus, with the appreciation that targeting innate immune function Correspondence to R.P.C.: robin.choudhury@cardiov.ox.ac.uk. Author contributionsAll the authors researched data for the article, discussed its contents, and wrote, reviewed, and edited the manuscript before submission. Competing interests statementThe authors declare no competing interests. HHS Public AccessAuthor manuscript Nat Rev Cardiol. Author manuscript; available in PMC 2017 September 01. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript in experimental models can variously attenuate disease progression and injury, and promote healing [7][8][9][10] .Processes of inflammation contribute to a broad range of cardiovascular diseases; however, in this Review, we consider the roles of inflammatory processes in the related pathologies of atherosclerosis and acute myocardial infarction (AMI), by providing an evaluation of known and emerging inflammatory pathways that are thought to be central to their pathogenesis, and the consequences of their activation. We highlight contemporary techniques to characterize and quantify inflammation, and consider h...

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Section: Atherosclerosis Pathogenesismentioning

confidence: 77%

Section: Atherosclerosis Pathogenesismentioning

confidence: 80%

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Ruparelia¹,

Chai²,

Fisher³

et al. 2017

Nat Rev Cardiol

194

View full text Add to dashboard Cite

show abstract

“…Interestingly, recent studies by our lab 6,7 and others 8,9 have begun to demonstrate that SMCs are capable of many more functions than those just related to contraction, dilation, and ECM deposition. The role of SMCs in alternative pathways is thought to be mediated through a process known as SMC phenotypic switching.…”

Section: List Of Figures and Legendsmentioning

confidence: 99%

“…Unlike it's cardiac muscle and skeletal muscle cousins, SMCs, although fully differentiated, are not terminally differentiated and in response to vascular injury 12,13 or disease [6][7][8] retain the capability to undergo phenotypic switching; a process characterized by coordinate and profound down regulation of SMC marker genes and upregulation of ECM synthesis, pluripotency genes, and migratory genes such as KLF4 6,14,15 and OCT4 7 . Although multiple SMC genes 10 have been described and used to identify SMCs in vivo, including smooth muscle alpha actin (ACTA2) 16 , smooth muscle myosin heavy chain (MYH11) 17 , h1-calponin 18 , and smooth muscle 22-alpha (TAGLN) 19 , phenotypic switching of SMCs is a process which is defined by down regulation (or loss) of these genes, making identification of phenotypically modulated SMCs in vivo exceedingly difficult using traditional methods which rely on gene or protein expression.…”

Section: Phenotypic Switchingmentioning

confidence: 99%

“…Future studies are needed to determine the effect of whole body irradiation on both early and late stage lesion development and defining the effect irradiation has on SMCs located in the lesion and the media of atherosclerotic vessels keeping in mind studies cannot rely on use of conventional SMC and macrophage marker genes to identify each of these respective cell types within lesions since each cell type can activate markers of the other cell type in the context of lesions 6,8 .…”

Section: The Subset Of Smcs That Proliferate In Response To Ligation mentioning

confidence: 99%

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Radiosensitive Smooth Muscle Cells Populate Neointimal Lesions Through a Platelet Derived Growth Factor Receptor Beta Dependent Mechanism

Griffith¹

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Vascular smooth muscle cell plasticity in the tumor microenvironment

Bell,

Baylis,

Lopez

et al. 2024

Cancer Communications

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Transdifferentiation of Vascular Smooth Muscle Cells to Macrophage-Like Cells During Atherogenesis

Cited by 465 publications

References 31 publications

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Radiosensitive Smooth Muscle Cells Populate Neointimal Lesions Through a Platelet Derived Growth Factor Receptor Beta Dependent Mechanism

Vascular smooth muscle cell plasticity in the tumor microenvironment

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