Role of Multislice CT in the Evaluation of Non-Vascular Complications Following Hepatic Transplantation from Adult Living Donors

Diabetes and its vascular complications affect an increasing number of people. This disease of epidemic proportion nowadays involves abnormalities of large and small blood vessels, all commencing with alterations of the endothelial cell (EC) functions. Cardiovascular diseases are a major cause of death and disability among diabetic patients. In diabetes, EC dysfunction (ECD) is induced by the pathological increase of glucose and by the appearance of advanced glycation end products (AGE) attached to the plasma proteins, including lipoproteins. AGE proteins interact with their specific receptors on EC plasma membrane promoting activation of signaling pathways, resulting in decreased nitric oxide bioavailability, increased intracellular oxidative and inflammatory stress, causing dysfunction and finally apoptosis of EC. Irreversibly glycated lipoproteins (AGE-Lp) were proven to have an important role in accelerating atherosclerosis in diabetes. The aim of the present review is to present up-to-date information connecting hyperglycemia, ECD and two classes of glycated Lp, glycated low-density lipoproteins and glycated high-density lipoproteins, which contribute to the aggravation of diabetes complications. We will highlight the role of dyslipidemia, oxidative and inflammatory stress and epigenetic risk factors, along with the specific mechanisms connecting them, as well as the new promising therapies to alleviate ECD in diabetes.

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Role of Asymmetric Dimethylarginine (ADMA) in Diabetic Vascular Complications

Current Pharmaceutical Design ◽

10.2174/138161208786071326 ◽

2008 ◽

Vol 14 (25) ◽

pp. 2613-2618 ◽

Cited By ~ 23

Author(s):

Sho-ichi Yamagishi ◽

Seiji Ueda ◽

Kazuo Nakamura ◽

Takanori Matsui ◽

Seiya Okuda

Keyword(s):

Asymmetric Dimethylarginine ◽

Vascular Complications ◽

Diabetic Vascular Complications

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Imaging of vascular complications after hepatic transplantation

American Journal of Roentgenology ◽

10.2214/ajr.150.6.1285 ◽

1988 ◽

Vol 150 (6) ◽

pp. 1285-1290 ◽

Cited By ~ 28

Author(s):

K Dalen ◽

DL Day ◽

NL Ascher ◽

DW Hunter ◽

WM Thompson ◽

...

Keyword(s):

Vascular Complications ◽

Hepatic Transplantation

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Role of vascular endothelial growth factor in diabetic vascular complications

Kidney International ◽

10.1046/j.1523-1755.2000.07718.x ◽

2000 ◽

Vol 58 ◽

pp. S113-S119 ◽

Cited By ~ 151

Author(s):

Lloyd Paul Aiello ◽

Jun-Shyan Wong

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Vascular Complications ◽

Vascular Endothelial ◽

Diabetic Vascular Complications ◽

Endothelial Growth Factor

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Protein Kinase C Activation, Development of Diabetic Vascular Complications, and Role of Vitamin E in Preventing These Abnormalities

Antioxidants in Diabetes Management ◽

10.1201/9781482277326-23 ◽

2000 ◽

pp. 267-290

Keyword(s):

Protein Kinase C ◽

Vitamin E ◽

Protein Kinase ◽

Vascular Complications ◽

Diabetic Vascular Complications ◽

Kinase C ◽

Protein Kinase C Activation

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The role of diabetes in the onset and development of endothelial dysfunction

Problems of Endocrinology ◽

10.14341/probl12212 ◽

2020 ◽

Vol 66 (1) ◽

pp. 47-55

Author(s):

Era B. Popyhova ◽

Tatiana V. Stepanova ◽

Dar’ya D. Lagutina ◽

Tatiana S. Kiriiazi ◽

Alexey N. Ivanov

Keyword(s):

Oxidative Stress ◽

Endothelial Dysfunction ◽

Critical Role ◽

Vascular Complications ◽

Glycation End Products ◽

Smooth Muscle Cell Migration ◽

Basic Functions ◽

Cell Migration And Proliferation ◽

Radical Processes

The vascular endothelium performs many functions. It is a key regulator of vascular homeostasis, maintains a balance between vasodilation and vasoconstriction, inhibition and stimulation of smooth muscle cell migration and proliferation, fibrinolysis and thrombosis, and is involved to regulation of platelet adhesion and aggregation. Endothelial dysfunction (ED) plays the critical role in pathogenesis of diabetes mellitus (DM) vascular complications. The purpose of this review was to consider the mechanisms leading to the occurrence of ED in DM. The paper discusses current literature data concerning the role of hyperglycemia, oxidative stress, advanced glycation end products in endothelial alteration. A separate section is devoted to the particularities of the functioning of the antioxidant system and their significance in the development of ED in DM. The analysis of the literature allows to conclude that pathological activation of glucose utilization pathways causes damage of endothelial cells, which is accompanied by disorders of all their basic functions. Metabolic disorders in DM cause a pronounced imbalance of free radical processes and antioxidant defense, accompanied by oxidative stress of endotheliocytes, which contributes to the progression of ED and the development of vascular complications. Many aspects of multicomponent regulatory reactions in the pathogenesis of the development of ED in DM have not been sufficiently studied.

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Abstract 357: Hepatic ERK2 Suppresses Endoplasmic Reticulum Stress, Leading to Protection from Oxidative Stress and Endothelial Dysfunction

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.33.suppl_1.a357 ◽

2013 ◽

Vol 33 (suppl_1) ◽

Author(s):

Takehiko Kujiraoka ◽

Yasushi Satoh ◽

Makoto Ayaori ◽

Yasunaga Shiraishi ◽

Yuko Arai-Nakaya ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Endoplasmic Reticulum ◽

Fatty Acid ◽

Endothelial Dysfunction ◽

Er Stress ◽

Vascular Complications ◽

Metabolic Remodeling ◽

And Oxidative Stress

Background Insulin signaling comprises 2 major cascades, the IRS/PI3K/Akt and Ras/Raf/MEK/ERK pathways. Many studies on the tissue-specific effects of the former pathway had been conducted, however, the role of the latter cascade in tissue-specific insulin resistance had not been investigated. High glucose/fatty acid toxicity, inflammation and oxidative stress, all of which are associated with insulin resistance, can activate ERK. Liver plays a central role of metabolism and hepatosteatosis (HST) is associated with vascular diseases. The aim of this study is to elucidate the role of hepatic ERK2 in HST, metabolic remodeling and endothelial dysfunction. Methods Serum biomarkers of vascular complications in human were compared between subjects with and without HST diagnosed by echography for regular medical checkup. Next, we created liver-specific ERK2 knockout mice (LE2KO) and fed them with a high-fat/high-sucrose diet (HFHSD) for 20 weeks. The histological analysis, the expression of hepatic sarco/endoplasmic reticulum (ER) Ca 2+ -ATPase 2 (SERCA2) and glucose-tolerance/insulin-sensitivity (GT/IS) were tested. Vascular superoxide production and endothelial function were evaluated with dihydroethidium staining and isometric tension measurement of aorta. Results The presence of HST significantly increased HOMA-IR, an indicator of insulin resistance or atherosclerotic index in human. HFHSD-fed LE2KO revealed a marked exacerbation in HST and metabolic remodeling represented by the impairment of GT/IS, elevated serum free fatty acid and hyperhomocysteinemia without changes in body weight, blood pressure and serum cholesterol/triglyceride levels. In the HFHSD-fed LE2KO, mRNA and protein expressions of hepatic SERCA2 were significantly decreased, which resulted in hepatic ER stress. Induction of vascular superoxide production and remarkable endothelial dysfunction were also observed in them. Conclusions Hepatic ERK2 revealed the suppression of hepatic ER stress and HST in vivo , which resulted in protection from vascular oxidative stress and endothelial dysfunction. HST with hepatic ER stress can be a prominent risk of vascular complications by metabolic remodeling and oxidative stress in obese-related diseases.

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