Vascular fibrosis in atherosclerosis

Lan, Tsuo Hung; Huang, Xiaofeng; Tan, Hongmei

doi:10.1016/j.carpath.2013.01.003

Cited by 132 publications

(117 citation statements)

References 119 publications

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“…Vascular fibrosis is associated with the renin-angiotensin-aldosterone system, oxidative stress, inflammatory cytokines, and the imbalance of endothelium-derived cytokine secretion (Lan et al, 2013). Gal-3 is a mediator of angiogenesis and plays a crucial role in vascular fibrosis (NangiaMakker et al, 2000;Mourad-Zeidan et al, 2008;Calvier et al, 2013).…”

Section: Gal-3 In Fibrotic Diseasesmentioning

confidence: 99%

Functions of Galectin-3 and Its Role in Fibrotic Diseases

Gao

2014

J Pharmacol Exp Ther

217

184

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Fibrotic diseases occur in a variety of organs and lead to continuous organ injury, function decline, and even failure. Currently effective treatment options are limited. Galectin-3 (Gal-3) is a pleiotropic lectin that plays an important role in cell proliferation, adhesion, differentiation, angiogenesis, and apoptosis. Accumulating evidence indicates that Gal-3 activates a variety of profibrotic factors, promotes fibroblast proliferation and transformation, and mediates collagen production. Recent studies have defined key roles for Gal-3 in fibrogenesis in diverse organ systems, including liver, kidney, lung, and myocardial. To help set the stage for future research, we review recent advances about the role played by Gal-3 in fibrotic diseases. Herein we discuss the potential profibrotic role of Gal-3, inhibition of which may represent a promising therapeutic strategy against tissue fibrosis.

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Section: Gal-3 In Fibrotic Diseasesmentioning

confidence: 99%

Functions of Galectin-3 and Its Role in Fibrotic Diseases

Gao

2014

J Pharmacol Exp Ther

217

184

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“…Vascular fibrosis is known to involve in the accumulation of ECM proteins, particularly collagen and fibronectin, and contributes to structural remodeling [33]. Excessive collagen or reduced elastin in the vascular wall leads to vascular fibrosis and increased stiffness [34].…”

Section: Discussionmentioning

confidence: 99%

“…CTGF is a downstream mediator of TGF-β1, and TGF-β1-induced CTGF expression is regulated by the Smad pathway [33,38]. CTGF is implicated in vascular remodeling by upregulation of extracellular matrix (ECM) [33,39], and CTGF overexpression promotes VSMCs to express more ECM protein [40].…”

Section: Discussionmentioning

confidence: 99%

Salusin-β contributes to vascular remodeling associated with hypertension via promoting vascular smooth muscle cell proliferation and vascular fibrosis

Sun

Liu

Zhang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Vascular smooth muscle cell (VSMC) proliferation and vascular fibrosis are closely linked with hypertension and atherosclerosis. Salusin-β is a bioactive peptide involved in the pathogenesis of atherosclerosis. However, it is still largely undefined whether salusin-β is a potential candidate in the VSMC proliferation and vascular fibrosis. Experiments were carried out in human vascular smooth muscle cells (VSMCs) and in rats with intravenous injection of lentivirus expressing salusin-β. In vitro, salusin-β promoted VSMCs proliferation, which was attenuated by adenylate cyclase inhibitor SQ22536, PKA inhibitor Rp-cAMP, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor AG1478, ERK inhibitor U0126 or cAMP response element binding protein (CREB) inhibitor KG501. It promoted the phosphorylation of ERK1/2, CREB and EGFR, which were abolished by SQ22536 or Rp-cAMP. Furthermore, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor AG1478 diminished the salusin-β-evoked ERK1/2 and CREB phosphorylation. On the other hand, salusin-β increased collagen-I, collagen-III, fibronectin and connective tissue growth factor (CTGF) mRNA and phosphorylation of Smad2/3, which were prevented by ALK5 inhibitor A83-01. In vivo, salusin-β overexpression increased the media thickness, media/lumen ratio coupled with ERK1/2, CREB, EGFR and Smad2/3 phosphorylation, as well as the mRNA of collagen-I, collagen-III, fibronectin, transforming growth factor-β1 (TGF-β1) and CTGF in arteries. Moreover, salusin-β overexpression in rats caused severe hypertension. Intravenous injection of salusin-β dose-relatedly increased blood pressure, but excessive salusin-β decreased blood pressure and heart rate. These results indicate that salusin-β promotes VSMC proliferation via cAMP-PKA-EGFR-CREB/ERK pathway and vascular fibrosis via TGF-β1-Smad pathway. Increased salusin-β contributes to vascular remodeling and hypertension.

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“…It has been shown in previous studies that adventitial fibroblasts play a significant role in inflammation of the arterial wall and pathogenesis of atherosclerosis (29,30). Lan et al (31) showed that TGF-β plays a critical role in extracellular matrix accumulation and vascular remodeling that is linked with many pathological progresses, including atherosclerosis. Dol-Gleizes et al (32) postulated that fibroblast growth factors have an important role in the development of vascular diseases like atherosclerosis and graft arteriosclerosis.…”

Section: Discussionmentioning

confidence: 99%

The Relationship between Proliferative Scars and Endothelial Function in Surgically Revascularized Patients

et al. 2015

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Background: Proliferative scars are benign fibrotic proliferations which demonstrate abnormal wound healing in response to skin injuries. As postulated in the "response to injury hypothesis", atherosclerosis is also triggered by an endothelial injury. Keloid and atherosclerotic processes have many pathophysiological and cytological features in common. Aims: In this study, we investigated the relationship between proliferative scars and endothelial function in surgically revascularized patients. We aimed to test the hypothesis that atherosclerosis is a wound healing abnormality. Study Design: Cross-sectional study. Methods: Consecutive patients who were admitted to the cardiology outpatient clinic with a history of coronary artery bypass grafting operation were evaluated. Thirty-three patients with proliferative scars at the median sternotomy site formed the keloid group, and 36 age-and sex-matched patients with no proliferative scar at the median sternotomy site formed the control group. Endothelial function was evaluated by flowmediated vasodilatation of the brachial artery via ultrasonograhic examination. Results: There is no signicant difference according to the demographic data, biochemical parameters, clinical parameters and number of grafts between keloid and control groups. Endothelial-dependent vasodilatory response was lower in the keloid group than the control group (9.30±3.5 and 18.68±8.2, respectively; p=0.001). Conclusion:This study showed that endothalial dysfunction, which is strongly correlated with atherosclerosis, was more prominent in patients with proliferative scars. As proliferative scars and atherosclerosis have many features in common, we might conclude that atherosclerosis is a wound healing abnormality.

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Vascular fibrosis in atherosclerosis

Cited by 132 publications

References 119 publications

Functions of Galectin-3 and Its Role in Fibrotic Diseases

Functions of Galectin-3 and Its Role in Fibrotic Diseases

Salusin-β contributes to vascular remodeling associated with hypertension via promoting vascular smooth muscle cell proliferation and vascular fibrosis

The Relationship between Proliferative Scars and Endothelial Function in Surgically Revascularized Patients

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