Vascular Aging and Vascular Disease Have Much in Common!

Watson, Anna; Chen, Yung-Chih; Peter, Karlheinz

doi:10.1161/atvbaha.122.317892

Cited by 7 publications

(8 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Probably, a synergistic action of all these elements reflects the different AAA phenotypes associated with BAV, as stressed in our works, than those detected in TAV individuals [4,10,12]. Differently, TAV subjects show a more advanced age of AAA onset, about versus the 70-75 years, and a pathogenesis more related to vascular aging and the resultant remodeling and degeneration process associated with a preeminent fibrosis, that significantly reduces the probability of AAA progression in dissection and rupture [2,[13][14][15][16][17]. Precisely, a typical vascular remodeling and degeneration, accompanied by wound healing associated with a significant increase of circulating EPC levels [9,11], tissue expression of TGF-β and Smad-3 [18][19][20][21] consequent inflammation, endothelial-to-mesenchymal transition (EndMT) [22][23][24] and fibrosis [25], embody aorta dilation, or better, AAA disease, in TAV patients.…”

Section: Introductionmentioning

confidence: 55%

The Endothelial Transcription Factor ERG Mediates a Differential Role in the Aneurysmatic Ascending Aorta with Bicuspid or Tricuspid Aorta Valve: A Preliminary Study

Pisano

Terriaca

Nardi

et al. 2022

IJMS

View full text Add to dashboard Cite

The pathobiology of ascending aorta aneurysms (AAA) onset and progression is not well understood and only partially characterized. AAA are also complicated in case of bicuspid aorta valve (BAV) anatomy. There is emerging evidence about the crucial role of endothelium-related pathways, which show in AAA an altered expression and function. Here, we examined the involvement of ERG-related pathways in the differential progression of disease in aortic tissues from patients having a BAV or tricuspid aorta valve (TAV) with or without AAA. Our findings identified ERG as a novel endothelial-specific regulator of TGF-β-SMAD, Notch, and NO pathways, by modulating a differential fibrotic or calcified AAA progression in BAV and TAV aortas. We provided evidence that calcification is correlated to different ERG expression (as gene and protein), which appears to be under control of Notch signaling. The latter, when increased, associated with an early calcification in aortas with BAV valve and aneurysmatic, was demonstrated to favor the progression versus severe complications, i.e., dissection or rupture. In TAV aneurysmatic aortas, ERG appeared to modulate fibrosis. Therefore, we proposed that ERG may represent a sensitive tissue biomarker to monitor AAA progression and a target to develop therapeutic strategies and influence surgical procedures.

show abstract

Section: Introductionmentioning

confidence: 55%

The Endothelial Transcription Factor ERG Mediates a Differential Role in the Aneurysmatic Ascending Aorta with Bicuspid or Tricuspid Aorta Valve: A Preliminary Study

Pisano

Terriaca

Nardi

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…Blood vessel disorders are related to events such as inflammation, atherosclerotic plaque, aneurysm, altered endothelial cell function, hypertension, or age. The sympathetic nervous system also exerts numerous potential indirect effects in vascular diseases [ 6 , 7 ]. It has been proposed that small vessel diseases are multisystem disorders with a common pathophysiological basis differentially affecting various organs.…”

Section: Spotlightmentioning

confidence: 99%

When it doesn't run in the blood(vessels) – events involved in vascular disorders

Kattner¹

2023

Biomedical Journal

View full text Add to dashboard Cite

“…Cardiovascular diseases (CVDs) are the leading cause of global death, with aging constituting a major risk factor . Age-related arterial stiffening and dysfunction is a precursor to the development of CVDs, such as hypertension, coronary heart disease, heart failure, and stroke. − The elasticity of the aorta allows it to distend during systole and then recoil during diastole, thus allowing for continuous blood flow and blood pressure regulation. During aging, arteries lose their elasticity via different mechanisms, including the loss of the elastin/collagen ratio, which leads to the loss of capacity to expand .…”

Section: Introductionmentioning

confidence: 99%

Studying the Synergistic Effect of Substrate Stiffness and Cyclic Stretch Level on Endothelial Cells Using an Elastomeric Cell Culture Chamber

Sekar

Suarez

Nguyen

et al. 2023

ACS Appl. Mater. Interfaces

Self Cite

View full text Add to dashboard Cite

Endothelial cells lining blood vessels are continuously exposed to biophysical cues that regulate their function in health and disease. As we age, blood vessels lose their elasticity and become stiffer. Vessel stiffness alters the mechanical forces that endothelial cells experience. Despite ample evidence on the contribution of endothelial cells to vessel stiffness, less is known about how vessel stiffness affects endothelial cells. In this study, we developed a versatile model to study the cooperative effect of substrate stiffness and cyclic stretch on human aortic endothelial cells. We cultured endothelial cells on elastomeric wells covered with fibronectin-coated polyacrylamide gel. Varying the concentrations of acrylamide and bis-acrylamide enabled us to produce soft and stiff substrates with elastic modules of 40 and 200 kPa, respectively. Using a customized three-dimensional (3D) printed cam-driven system, the cells were exposed to 5 and 10% cyclic stretch levels. This enabled us to mimic the stiffness and stretch levels that endothelial cells experience in young and aged arteries. Using this model, we found that endothelial cells cultured on a soft substrate had minimal cytoskeletal alignment to the direction of the stretch compared to the ones cultured on the stiff substrate. We also observed an increase in the cellular area and aspect ratio in cells cultured on the stiff substrate, both of which are positively regulated by cyclic stretch. However, neither cyclic stretch nor substrate stiffness significantly affected the nuclear circularity. Additionally, we found that the accumulation of NF-κB in the nucleus, endothelial proliferation, tube formation, and expression of IL1β depends on the stretch level and substrate stiffness. Our model can be further used to investigate the complex signaling pathways associated with vessel stiffening that govern the endothelial responses to mechanical forces.

show abstract

Vascular Aging and Vascular Disease Have Much in Common!

Cited by 7 publications

References 48 publications

The Endothelial Transcription Factor ERG Mediates a Differential Role in the Aneurysmatic Ascending Aorta with Bicuspid or Tricuspid Aorta Valve: A Preliminary Study

The Endothelial Transcription Factor ERG Mediates a Differential Role in the Aneurysmatic Ascending Aorta with Bicuspid or Tricuspid Aorta Valve: A Preliminary Study

When it doesn't run in the blood(vessels) – events involved in vascular disorders

Studying the Synergistic Effect of Substrate Stiffness and Cyclic Stretch Level on Endothelial Cells Using an Elastomeric Cell Culture Chamber

Contact Info

Product

Resources

About