Atherosclerosis

2012

DOI: 10.1016/j.atherosclerosis.2011.10.003

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Increased thrombospondin-2 in human fibrosclerotic and stenotic aortic valves

Virva Pohjolainen

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³

et al.

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Introduction3

Other Processes Associated With Avc1

Thrombospondins1

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Cited by 32 publications

(33 citation statements)

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“…65 There is also evidence of increased thrombospondin-2, a matricellular protein that regulates extracellular matrix remodeling and fibrosis in human fibrocalcific aortic valve disease as well as the profibrotic enzyme neutral endopeptidase. 66, 67 …”

Section: Other Processes Associated With Avcmentioning

confidence: 99%

Cellular Mechanisms of Aortic Valve Calcification

¹

2012

Circ: Cardiovascular Interventions

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Acquired aortic valve disease and valvular calcification is highly prevalent in adult populations worldwide and is associated with significant cardiovascular morbidity and mortality. At present, there are no medical therapies that will prevent or regress aortic valve calcification or stenosis and surgical or transcatheter aortic valve replacement remain the only effective therapies for treating this disease. In the setting of valve injury as a result of exposure to biochemical mediators or hemodynamic forces, normal homeostatic processes are disrupted resulting in extracellular matrix degradation, aberrant matrix deposition and fibrosis, inflammatory cell infiltration, lipid accumulation, and neoangiogenesis of the valve tissue and, ultimately, calcification of the valve. Calcification of the aortic valve is now understood to be an active process that involves the coordinated actions of resident valve endothelial and interstitial cells, circulating inflammatory and immune cells, and bone marrow-derived cells. These cells may undergo a phenotype transition to become osteoblast-like cells and elaborate bone matrix, endothelial-to-mesenchymal transition, and form matrix vesicles that serve as a nidus for microcalcifications. Each of these mechanisms has been shown to contribute to aortic valve calcification suggesting that strategies that target these cellular events may lead to novel therapeutic interventions to halt the progression or reverse aortic valve calcification.

“…65 There is also evidence of increased thrombospondin-2, a matricellular protein that regulates extracellular matrix remodeling and fibrosis in human fibrocalcific aortic valve disease as well as the profibrotic enzyme neutral endopeptidase. 66, 67 …”

Section: Other Processes Associated With Avcmentioning

confidence: 99%

Cellular Mechanisms of Aortic Valve Calcification

¹

2012

Circ: Cardiovascular Interventions

View full text Add to dashboard Cite

Acquired aortic valve disease and valvular calcification is highly prevalent in adult populations worldwide and is associated with significant cardiovascular morbidity and mortality. At present, there are no medical therapies that will prevent or regress aortic valve calcification or stenosis and surgical or transcatheter aortic valve replacement remain the only effective therapies for treating this disease. In the setting of valve injury as a result of exposure to biochemical mediators or hemodynamic forces, normal homeostatic processes are disrupted resulting in extracellular matrix degradation, aberrant matrix deposition and fibrosis, inflammatory cell infiltration, lipid accumulation, and neoangiogenesis of the valve tissue and, ultimately, calcification of the valve. Calcification of the aortic valve is now understood to be an active process that involves the coordinated actions of resident valve endothelial and interstitial cells, circulating inflammatory and immune cells, and bone marrow-derived cells. These cells may undergo a phenotype transition to become osteoblast-like cells and elaborate bone matrix, endothelial-to-mesenchymal transition, and form matrix vesicles that serve as a nidus for microcalcifications. Each of these mechanisms has been shown to contribute to aortic valve calcification suggesting that strategies that target these cellular events may lead to novel therapeutic interventions to halt the progression or reverse aortic valve calcification.

“…Increased TSP-1 expression is also often found in tissue growth and remodeling, e.g., in embryo fibroblasts in response to c-Jun stimulation (135). Increased levels of TSP-1 and TSP-2 have been reported in remodeling large arteries in atherosclerotic lesions and after injury (13, 35, 51, 80). …”

Section: Introductionmentioning

confidence: 99%

Invoking the power of thrombospondins: Regulation of thrombospondins expression

Stenina‐Adognravi¹

2014

Matrix Biology

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Increasing evidence suggests critical functions of thrombospondins (TSPs) in a variety of physiological and pathological processes. With the growing understanding of the importance of these matricellular proteins, the need to understand the mechanisms of regulation of their expression and potential approaches to modulate their levels is also increasing. The regulation of TSPs expression is multi-leveled, cell- and tissue-specific, and very precise. However, the knowledge of mechanisms modulating the levels of TSPs is fragmented and incomplete. This review discusses the known mechanisms of regulation of TSPs levels and the gaps in our knowledge that prevent us from developing strategies to modulate the expression of these physiologically important proteins.

“…In a mouse cardiomyocyte grafting model, lack of TSP2 led to reduced fibrosis and peri-graft scar thickness, while endothelial cell density and cardiomyocyte graft size were increased (26). Moreover, TSP2 was the only TSP increased in fibrosclerotic and stenotic aortic valves of patients with calcific aortic valve disease, expressed in valvular myofibroblasts and neovessels (27). In patients with systemic sclerosis (SSc), TSP2 serum levels were increased and correlated with the severity of the disease.…”

Section: Thrombospondinsmentioning

confidence: 99%

Matricellular Proteins and Organ Fibrosis

¹

,

²

2017

Curr Pathobiol Rep

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All reported studies/experiments with human or animal subjects performed by the authors have been previously published and complied with all applicable ethical standards (including the Helsinki declaration and its amendments, institutional/national research committee standards, and international/national/institutional guidelines).

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