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Arteriosclerosis

The Experts below are selected from a list of 213 Experts worldwide ranked by ideXlab platform

Qingbo Xu – 1st expert on this subject based on the ideXlab platform

  • stem cells and transplant Arteriosclerosis
    Circulation Research, 2008
    Co-Authors: Qingbo Xu

    Abstract:

    Stem cells can differentiate into a variety of cells to replace dead cells or to repair damaged tissues. Recent evidence indicates that stem cells are involved in the pathogenesis of transplant Arteriosclerosis, an alloimmune initiated vascular stenosis that often results in transplant organ failure. Although the pathogenesis of transplant Arteriosclerosis is not yet fully understood, recent developments in stem cell research have suggested novel mechanisms of vascular remodeling in allografts. For example, stem cells derived from the recipient may repair damaged endothelial cells of arteries in transplant organs. Further evidence suggests that stem cells or endothelial progenitor cells may be released from both bone marrow and non–bone marrow tissues. Vascular stem cells appear to replenish cells that died in donor vessels. Concomitantly, stem/progenitor cells may also accumulate in the intima, where they differentiate into smooth muscle cells. However, several issues concerning the contribution of stem cells to the pathogenesis of transplant Arteriosclerosis are controversial, eg, whether bone marrow–derived stem cells can differentiate into smooth muscle cells that form neointimal lesions of the vessel wall. This review summarizes recent research on the role of stem cells in transplant Arteriosclerosis, discusses the mechanisms of stem cell homing and differentiation into mature endothelial and smooth muscle cells, and highlights the controversial issues in the field.

  • mouse models of Arteriosclerosis from arterial injuries to vascular grafts
    American Journal of Pathology, 2004
    Co-Authors: Qingbo Xu

    Abstract:

    Animal models are designed to be preliminary tools for better understanding of the pathogenesis, improvement in diagnosis, prevention, and therapy of Arteriosclerosis in humans. Attracted by the well-defined genetic systems, a number of investigators have begun to use the mouse as an experimental system for Arteriosclerosis research. Hundreds of inbred lines have been established, and the genetic map is relatively well defined, and both congenic strains and recombinant strains are available to facilitate genetic experimentation. Because Arteriosclerosis is a complicated disease, which includes spontaneous (native) atherosclerosis, transplant Arteriosclerosis, vein graft atherosclerosis, and angioplasty-induced restenosis, several mouse models for studying all types of Arteriosclerosis have recently been established. Using these mouse models, much knowledge concerning the pathogenesis of the disease and therapeutic intervention has been gained, eg, origins of endothelial and smooth muscle cells in lesions of transplant and vein graft atherosclerosis. This review will not attempt to cover all aspects of mouse models, rather focus on models of arterial injuries, vein grafts, and transplant Arteriosclerosis, by which the major progress in understanding the mechanisms of the disease has been made. This article will also point out (dis)advantages of a variety of models, and how the models can be appropriately chosen for different purposes of study.

  • Smooth muscle cell apoptosis in Arteriosclerosis.
    Experimental Gerontology, 2001
    Co-Authors: Manuel Mayr, Qingbo Xu

    Abstract:

    Abstract Arteriosclerosis, a paradigmatic age-related disease, encompasses (spontaneous) atherosclerosis, restenosis after percutaneous transluminal coronary angioplasty, autologous arterial or vein graft Arteriosclerosis and transplant Arteriosclerosis. In all types of Arteriosclerosis, vascular smooth muscle cell (SMC) accumulation in the intima is a key event, but abundant evidence also indicates the importance of SMC apoptosis in the development of Arteriosclerosis. Because SMC proliferation and apoptosis coincide in arteriosclerotic lesions, the balance between these two processes could be a determinant during vessel remodeling and disease development. Various stimuli, including oxidized lipoproteins, altered hemodynamic stress and free radicals, can induce SMC apoptosis in vitro. As risk factors for Arteriosclerosis, these stimuli may also lead to vascular cell apoptosis in vivo. The presence of apoptotic cells in atherosclerotic and restenotic lesions could have potential clinical implications for atherogenesis and contributes to the instability of the lesion. Based on the progress in this field, this review focuses on the mechanism and impact of SMC apoptosis in the pathogenesis of Arteriosclerosis and highlights the role of biomechanical stress in SMC apoptosis.

Markus Van Der Giet – 2nd expert on this subject based on the ideXlab platform

  • Arteriosclerosis and vascular calcification causes clinical assessment and therapy
    European Journal of Clinical Investigation, 2015
    Co-Authors: Markus Tolle, Alexander Reshetnik, Mirjam Schuchardt, Matthias Hohne, Markus Van Der Giet

    Abstract:

    Background

    Arteriosclerosis is a pathological, structural (media vascular calcification) and physiological (modified vascular smooth vessel cells; increased arterial stiffness) alteration of the vessel wall. Through improved assessment methods (functional and imaging), it has become a well-known phenomenon in recent decades. However, its clinical importance was underestimated until recently.

    Materials and methods

    Currently available English-speaking data about conditions/diseases associated with Arteriosclerosis, its clinical sequels, available diagnostic procedures and therapeutic modalities were reviewed and summarized.

    Results

    In recent decades, emerging data have brought about a better understanding of causes and consequences of Arteriosclerosis and highlight its growing clinical impact.

    Conclusion

    Although Arteriosclerosis showed an independent clinical impact on cardiovascular morbidity and mortality, especially in patients with chronic kidney disease/end-stage renal disease (CKD/ESRD) and diabetes mellitus, convincing clinical therapy concepts are not available until now. The establishment of novel therapeutic strategies derived from basic research is strongly needed.

Kohji Shirai – 3rd expert on this subject based on the ideXlab platform

  • estimating the extent of subclinical Arteriosclerosis of persons with prediabetes and diabetes mellitus among japanese urban workers and their families a cross sectional study
    BMC Cardiovascular Disorders, 2016
    Co-Authors: Tsukasa Namekata, Kohji Shirai, Kenji Suzuki, Naohito Tanabe, Kunio Miyanishi, Mitsuko Nakata, Chikao Arai, Norio Ishizuka

    Abstract:

    Diabetes mellitus (hereafter called diabetes) is considered to accelerate Arteriosclerosis leading to coronary heart disease and stroke. Thus, it is important to quantitatively estimate the extent of subclinical Arteriosclerosis. A new method called cardio-ankle vascular index (CAVI) is developed to reflect arterial stiffness independently from blood pressure at the time of measurement. Then, we examined if CAVI scores could discriminate the extent of Arteriosclerosis between persons with prediabetes (or borderline diabetes) and with diabetes among Japanese urban workers and their families. Subjects were 9881 men and 12033 women of company employees and their families who participated in cardiovascular disease screening in Japan. Persons having diabetes and prediabetes were defined based on the criteria set by American Diabetes Association. CAVI scores were measured by VaSera VS-1000. We applied the established age-sex specific cutoff points of CAVI scores above which were determined to be abnormally high or advanced level of Arteriosclerosis. To examine the association of prediabetes and diabetes with CAVI scores, CAVI scores of screening participants were converted to a binary variable: 1 for less than cutoff points and 2 for equal or greater than cutoff points or abnormally high CAVI scores. Logistic regression method was used to examine the association of prediabetes and diabetes with CAVI scores after adjusting for major cardiovascular disease (CVD) risk factors. Prevalence of abnormally high CAVI scores was significantly higher after 40 years of age among persons with diabetes than either among persons with prediabetes or among normal persons in both genders. Significantly elevated odds ratios (ORs) of abnormally high CAVI scores appeared among persons with prediabetes: 1.29 (95 % confidence interval (CI), 1.11-1.48) for men and 1.14 (CI, 1.01-1.28) for women, and among persons with diabetes: 2.41 (CI, 1.97-2.95) for men and 2.52 (CI, 1.94-3.28) for women. The extent of subclinical Arteriosclerosis (including arterial stiffness and atherosclerosis) was moderately enhanced among persons with prediabetes and was further advanced among persons with diabetes. Thus, it is important to introduce earlier interventions for changing lifestyle and diet of persons with prediabetes in order to prevent them from developing diabetes and further advancing Arteriosclerosis.

  • establishing baseline criteria of cardio ankle vascular index as a new indicator of Arteriosclerosis a cross sectional study
    BMC Cardiovascular Disorders, 2011
    Co-Authors: Tsukasa Namekata, Kenji Suzuki, Norio Ishizuka, Kohji Shirai

    Abstract:

    Background
    A cardio-ankle vascular index (CAVI) has been developed to represent the extent of Arteriosclerosis throughout the aorta, femoral artery and tibial artery independent of blood pressure. To practically use CAVI as a diagnostic tool for determining the extent of Arteriosclerosis, our study objectives were (1) to establish the baseline CAVI scores by age and gender among cardiovascular disease (CVD) risk-free persons, (2) to compare CAVI scores between genders to test the hypothesis that the extent of Arteriosclerosis in men is greater than in women, and (3) to compare CAVI scores between the CVD risk-free group and the CVD high-risk group in order to test the hypothesis that the extent of Arteriosclerosis in the CVD high-risk group is greater than in the CVD risk-free group.