The role of endothelial dysfunction and oxidative stress in cerebrovascular diseases

Scicchitano, Pietro; Cortese, Francesca; Gesualdo, Michele; Palo, Micaela De; Massari, Francesco; Giordano, Paola; Ciccone, Marco Matteo

doi:10.1080/10715762.2019.1620939

Cited by 41 publications

(30 citation statements)

References 158 publications

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“…We create a chip to fabricate and perfuse four TEBVs simultaneously and develop a three-layer model of ECs, SMCs, and fibroblasts. Endothelial dysfunction is an early step in atherosclerosis and plays a central role in many vascular-related disorders [32][33][34] . Similar to natural blood vessels, functional properties of tissueengineered vessels are highly dependent on the endothelial layer 35,36 .…”

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confidence: 99%

Modeling early stage atherosclerosis in a primary human vascular microphysiological system

et al. 2020

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Novel atherosclerosis models are needed to guide clinical therapy. Here, we report an in vitro model of early atherosclerosis by fabricating and perfusing multi-layer arteriole-scale human tissue-engineered blood vessels (TEBVs) by plastic compression. TEBVs maintain mechanical strength, vasoactivity, and nitric oxide (NO) production for at least 4 weeks. Perfusion of TEBVs at a physiological shear stress with enzyme-modified low-density-lipoprotein (eLDL) with or without TNFα promotes monocyte accumulation, reduces vasoactivity, alters NO production, which leads to endothelial cell activation, monocyte accumulation, foam cell formation and expression of pro-inflammatory cytokines. Removing eLDL leads to recovery of vasoactivity, but not loss of foam cells or recovery of permeability, while pretreatment with lovastatin or the P2Y11 inhibitor NF157 reduces monocyte accumulation and blocks foam cell formation. Perfusion with blood leads to increased monocyte adhesion. This atherosclerosis model can identify the role of drugs on specific vascular functions that cannot be assessed in vivo.

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confidence: 99%

Modeling early stage atherosclerosis in a primary human vascular microphysiological system

et al. 2020

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“…Furthermore, investigation in patients with chronic periodontitis demonstrated that endothelial dysfunction of the branchial artery occurred with greater frequency in patients with periodontitis than in those without periodontitis [46]. Interestingly, this study and other investigators showed that together with various cytokines and inflammation-related molecules, oxidative stress regulated the relationship between periodontitis and endothelial dysfunction [49,50].…”

Section: Modulators Of Periodontal Diseasementioning

confidence: 74%

Pathological Characteristics of Periodontal Disease in Patients with Chronic Kidney Disease and Kidney Transplantation

Kitamura

Mochizuki

Miyata

et al. 2019

IJMS

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Chronic kidney disease (CKD) is recognized as an irreversible reduction of functional nephrons and leads to an increased risk of various pathological conditions, including cardiovascular disease and neurological disorders, such as coronary artery calcification, hypertension, and stroke. In addition, CKD patients have impaired immunity against bacteria and viruses. Conversely, kidney transplantation (KT) is performed for patients with end-stage renal disease as a renal replacement therapy. Although kidney function is almost normalized by KT, immunosuppressive therapy is essential to maintain kidney allograft function and to prevent rejection. However, these patients are more susceptible to infection due to the immunosuppressive therapy required to maintain kidney allograft function. Thus, both CKD and KT present disadvantages in terms of suppression of immune function. Periodontal disease is defined as a chronic infection and inflammation of oral and periodontal tissues. Periodontal disease is characterized by the destruction of connective tissues of the periodontium and alveolar bone, which may lead to not only local symptoms but also systemic diseases, such as cardiovascular diseases, diabetes, liver disease, chronic obstructive pulmonary disease, and several types of cancer. In addition, the prevalence and severity of periodontal disease are significantly associated with mortality. Many researchers pay special attention to the pathological roles and clinical impact of periodontal disease in patients with CKD or KT. In this review, we provide information regarding important modulators of periodontal disease to better understand the relationship between periodontal disease and CKD and/or KT. Furthermore; we evaluate the impact of periodontal disease on various pathological conditions in patients with CKD and KT. Moreover, pathogens of periodontal disease common to CKD and KT are also discussed. Finally, we examine the importance of periodontal care in these patients. Thus, this review provides a comprehensive overview of the pathological roles and clinical significance of periodontal disease in patients with CKD and KT.

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“…According to numerous studies both in vitro and in vivo, oxidative stress makes changes in homeostasis, which impairs functionality of vascular endothelia [32][33][34]. B[a]P, which is a major environmental carcinogen, causes DNA damage by promoting oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Kirenol Inhibits B[a]P‐Induced Oxidative Stress and Apoptosis in Endothelial Cells via Modulation of the Nrf2 Signaling Pathway

Rajendran

Ahmed

Veeraraghavan

2021

Oxidative Medicine and Cellular Longevity

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Atherosclerosis is a persistent inflammatory disorder specified by the dysfunction of the arteries, the world’s leading cause of cardiovascular diseases. We sought to determine the effectiveness of KRL in B[a]P-induced oxidative stress and programmed cell death in endothelial cells. Western blotting, real-time PCR, DCFH2-DA, and TUNEL staining were performed to detect pPI3K, pAKT, Nrf2, HO-1, NQO-1, Bcl2, Bax, and caspase-3 on the HUVECs. Through the pretreatment of KRL, a drastic enhancement was observed in the cell viability of HUVECs, whereas DNA damage and generation of reactive oxygen species induced by B[a]P was suppressed. KRL’s potential use as an antioxidant was observed to have a direct correlation with an antioxidant gene’s augmented expression and the nuclear translocation activation of Nrf2, even during the event when B[a]P was found to be absent. In addition, this study proved that the signaling cascades of PI3K/AKT mediated Nrf2 translocation. Activation of suppressed nuclear Nrf2 and reduced antioxidant genes across cells interacting with an LY294002 confirmed this phenomenon. In addition, knockdown of Nrf2 by Nrf2-siRNA transfection abolished the protective effects of KRL on HUVECs cells against oxidative damage. Finally, the expression of apoptotic proteins also supported the hypothesis that KRL may inhibit endothelial dysfunction. This study showed that KRL potentially prevents B[a]P-induced redox imbalance in the vascular endothelium by inducing the Nrf2 signaling via the PI3K/AKT pathway.

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The role of endothelial dysfunction and oxidative stress in cerebrovascular diseases

Cited by 41 publications

References 158 publications

Modeling early stage atherosclerosis in a primary human vascular microphysiological system

Modeling early stage atherosclerosis in a primary human vascular microphysiological system

Pathological Characteristics of Periodontal Disease in Patients with Chronic Kidney Disease and Kidney Transplantation

Kirenol Inhibits B[a]P‐Induced Oxidative Stress and Apoptosis in Endothelial Cells via Modulation of the Nrf2 Signaling Pathway

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