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Relevant bibliographies by topics / Neovascularization. Cell adhesion. Extracellular matrix / Books

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Books on the topic 'Neovascularization. Cell adhesion. Extracellular matrix'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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Consult the top 19 books for your research on the topic 'Neovascularization. Cell adhesion. Extracellular matrix.'

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1

Shrestha, Prashanta. Tenascin: An extracellular matrix protein in cell growth, adhesion and cancer. Chapman & Hall, 1997.

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2

C, Adams Josephine, and American Society for Cell Biology., eds. Methods in cell-matrix adhesion. Academic Press, 2002.

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3

Thomas, Kreis, and Vale Ronald, eds. Guidebook to the extracellular matrix, anchor, and adhesion proteins. 2nd ed. Oxford University Press, 1999.

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4

Thomas, Kreis, and Vale Ronald, eds. Guidebook to the extracellular matrix and adhesion proteins. Oxford University Press, 1993.

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5

Adams, Josephine. Methods in Cell-Matrix Adhesion (Methods in Cell Biology, Volume 69). Academic Press, 2002.

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6

(Editor), David A. Cheresh, and Robert P. Mecham (Series Editor), eds. Integrins: Molecular and Biological Responses to the Extracellular Matrix (Biology of Extracellular Matrix). Academic Press, 1994.

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7

(Editor), David A. Cheresh, and Robert P. Mecham (Series Editor), eds. Integrins: Molecular and Biological Responses to the Extracellular Matrix (Biology of Extracellular Matrix). Academic Press, 1994.

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8

Cell adhesion molecules and matrix proteins: Role in health and diseases. Landes, 1998.

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9

Macieira-Coelho, Alvaro. Signaling Through the Cell Matrix. Springer, 2000.

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10

Heino, Jyrki, and Veli-matti Kahari. Cell Invasion (Medical Intelligence Unit). Landes Bioscience, 2002.

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11

Crossin, Kathryn L. Tenascin and Counteradhesive Molecules of the Extracellular Matrix (Cell Adhesion and Communication Series). CRC, 1996.

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12

A, Cheresh David, and Mecham Robert P, eds. Integrins: Molecular and biological responses to the extracellular matrix. Academic Press, 1994.

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13

Shrestha, Prashanta, and Masahiko Mori. Tenascin: An Extracellular Matrix Protein in Cell Growth, Adhesion and Cancer (Molecular Biology Intelligence Unit). Springer, 1998.

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14

Shrestha, Prashanta, and Masahiko Mori. Tenascin: An Extracellular Matrix Protein in Cell Growth, Adhesion and Cancer (Molecular Biology Intelligence Unit). Chapman & Hall, 1997.

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15

Gregory, Bock, Clark Sarah, and Ciba Foundation, eds. Junctional complexes of epithelial cells. Wiley, 1987.

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16

Cheng, C. Y. The Molecular Mechanisms in Spermatogenesis. Landes Bioscience, 2007.

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17

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

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18

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Abstract:

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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19

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

Full text

Abstract:

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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