Endothelial glycocalyx and severity and vulnerability of coronary plaque in patients with coronary artery disease

Nemoto, Teruyoshi; Minami, Yoshiyasu; Yamaoka‐Tojo, Minako; Kato, Ayami; Katsura, Aritomo; Sato, Toshimitsu; Muramatsu, Yusuke; Kakizaki, Ryota; Fujiyoshi, Kazuhiro; Hashimoto, Takuya; Meguro, Kentaro; Shimohama, Takao; Ako, Junya

doi:10.1016/j.atherosclerosis.2020.04.014

Cited by 18 publications

(14 citation statements)

References 28 publications

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“…Compared to the rapid increase of circulating fragmented glycocalyx levels in acute diseases, circulating levels of fragmented glycocalyx was reduced in patients with chronic pathological conditions such as stable angina 47 . In such a pathological condition, thinning of the glycocalyx layer and reduction of the blood level of fragmented glycocalyx occur simultaneously due to the decreased production and accelerated degradation of the vascular endothelial glycocalyx.…”

Section: Ischemic Heart Diseasementioning

confidence: 88%

Mechanism of Vascular Endothelial Dysfunction Causing Arteriosclerosis: Vascular Endothelial Glycocalyx

Yamaoka‐Tojo¹

2020

Preprint

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In atherosclerosis patients, vascular endothelial dysfunction is commonly observed with damage of vascular endothelial glycocalyx, an extracellular matrix-bound to and encapsulating the endothelial cell lining the blood vessel wall. Unfavorable lifestyle; smoking and physical inactivity, also induces glycocalyx degradation. Moreover, the vascular endothelial glycocalyx is damaged by various unfavorable disease conditions like as dehydration, acute infectious disease, trauma, sepsis, ARDS, Kawasaki disease, preeclampsia, gestational diabetes mellitus, hypertension, diabetes, chronic kidney disease, atherosclerosis, stroke, dementia, microvascular angina, acute coronary syndrome, and heart failure. The vascular endothelial glycocalyx has been shown to be important not only as a physical cytoprotective barrier for vascular endothelial cells but also as a mechanism that regulates intracellular cell signaling. Therefore, vascular endothelial glycocalyx has great potential to explore new strategies for assessing the benefit conditions of our healthy vasculature.

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Section: Ischemic Heart Diseasementioning

confidence: 88%

Mechanism of Vascular Endothelial Dysfunction Causing Arteriosclerosis: Vascular Endothelial Glycocalyx

Yamaoka‐Tojo¹

2020

Preprint

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“…Breakdown of the eGC has been investigated in the etiology of cardiovascular disease, and increasing evidence has demonstrated a link between eGC shedding and the development of acute and chronic organ failure 2 , 15 . Because degradation of the eGC is induced by both cellular insults and clinical events, several clinically relevant in vitro and in vivo research models have been established to further study eGC damage using ischemia–reperfusion injury, tumor necrosis factor (TNF)-α administration, oxidative stress, and active eGC degradation enzymes (e.g.…”

Section: Discussionmentioning

confidence: 99%

Heparanase inhibition preserves the endothelial glycocalyx in lung grafts and improves lung preservation and transplant outcomes

Noda

Philips

Snyder

et al. 2021

Sci Rep

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The endothelial glycocalyx (eGC) is considered a key regulator of several mechanisms that prevent vascular injury and disease. Degradation of this macromolecular layer may be associated with post-transplant graft dysfunction. In this study, we aimed to demonstrate the benefits of eGC protection via heparanase inhibition on graft quality. We established rat models of lung grafts with damaged or preserved eGC using ischemic insult and transplanted the grafts into recipients. Lung grafts were also subjected to normothermic ex vivo lung perfusion for detailed assessment under isolated conditions. Physiologic parameters and eGC-associated cellular events were assessed in grafts before and after reperfusion. Structurally degraded eGC and highly activated heparanase were confirmed in lungs with ischemic insult. After transplant, lungs with damaged eGC exhibited impaired graft function, inflammation, edema, and inflammatory cell migration. Increased eGC shedding was evident in the lungs after reperfusion both in vivo and ex vivo. These reperfusion-related deficiencies were significantly attenuated in lungs with preserved eGC following heparanase inhibition. Our studies demonstrated that eGC plays a key role in maintaining lung graft quality and function. Heparanase inhibition may serve as a potential therapeutic to preserve eGC integrity, leading to improved post-transplant outcomes.

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“…Based on these findings, the circulating syndecan-1 level may be considered a diagnostic biomarker of destabilized coronary plaque. Compared with the rapid increase in circulating fragmented glycocalyx levels in acute diseases, circulating fragmented glycocalyx levels in patients with chronic pathological conditions such as stable angina were low [57]. In such pathological conditions, thinning of the glycocalyx layer and reduction of the blood level of fragmented glycocalyx occur simultaneously because of the de-creased production and accelerated degradation of the vascular endothelial glycocalyx.…”

Section: Ischemic Heart Diseasementioning

confidence: 94%

Vascular Endothelial Glycocalyx as a Mechanism of Vascular Endothelial Dysfunction and Atherosclerosis

Yamaoka‐Tojo¹

2020

WJCD

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Atherosclerosis occurs as a result of organized processes that include vascular endothelial dysfunction, lipid accumulation, abnormal inflammatory reaction, excessive reactive oxygen species production, and vascular cell proliferation and migration. In patients with atherosclerosis, vascular endothelial dysfunction is commonly observed with the damage of vascular endothelial glycocalyx, which is an extracellular matrix bound to and encapsulating the endothelial cells that line the blood vessel wall. Unhealthy lifestyle choices such as smoking and physical inactivity also induce glycocalyx degradation. Additionally, vascular endothelial glycocalyx can be damaged by various pathological conditions including dehydration, acute infectious disease, trauma, sepsis, acute respiratory distress syndrome, Kawasaki disease, preeclampsia, gestational diabetes mellitus, hypertension, diabetes mellitus, chronic kidney disease, atherosclerosis, stroke, dementia, microvascular angina, acute coronary syndrome, and heart failure. Vascular endothelial glycocalyx has been shown to be important as a physical cytoprotective barrier for vascular endothelial cells and as a regulatory mechanism for intracellular cell signaling. Therefore, vascular endothelial glycocalyx has immense potential in the exploration of novel strategies for the evaluation of beneficial conditions of healthy vasculature.

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Endothelial glycocalyx and severity and vulnerability of coronary plaque in patients with coronary artery disease

Abstract: Serum syndecan-1 level is not associated with angiographic coronary severity.• Lower syndecan-1 is associated with higher prevalence of vulnerable plaque.• Impairment of glycocalyx might be involved in the development of vulnerable plaque.

Cited by 18 publications

References 28 publications

Mechanism of Vascular Endothelial Dysfunction Causing Arteriosclerosis: Vascular Endothelial Glycocalyx

Mechanism of Vascular Endothelial Dysfunction Causing Arteriosclerosis: Vascular Endothelial Glycocalyx

Heparanase inhibition preserves the endothelial glycocalyx in lung grafts and improves lung preservation and transplant outcomes

Vascular Endothelial Glycocalyx as a Mechanism of Vascular Endothelial Dysfunction and Atherosclerosis

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