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This volume of the series Cardiac and Vascular Biology presents the most relevant aspects of vascular mechanobiology along with many more facets of this fascinating, timely and clinically highly relevant field. Mechanotransduction, mechanosensing, fluid shear stress, hameodynamics and cell fate, are just a few topics to name. All important aspects of vascular mechanobiology in health and disease are reviewed by some of the top experts in the field. This volume, together with a second title on cardiac mechanobiology featured in this series, will be of high relevance to scientists and clinical researchers in the area of vascular biology, cardiology and biomedical engineering.
Mechanobiology in Health and Disease brings together contributions from leading biologists, clinicians, physicists and engineers in one convenient volume, providing a unified source of information for researchers in this highly multidisciplinary area. Opening chapters provide essential background information on cell mechanotransduction and essential mechanobiology methods and techniques. Other sections focus on the study of mechanobiology in healthy systems, including bone, tendons, muscles, blood vessels, the heart and the skin, as well as mechanobiology studies of pregnancy. Final chapters address the nascent area of mechanobiology in disease, from the study of bone conditions, skin diseases and heart diseases to cancer. A discussion of future perspectives for research completes each chapter in the volume. This is a timely resource for both early-career and established researchers working on mechanobiology. - Provides an essential digest of primary research from many fields and disciplines in one convenient volume - Covers both experimental approaches and descriptions of mechanobiology problems from mathematical and numerical perspectives - Addresses the hot topic of mechanobiology in disease, a particularly dynamic field of frontier science
The book represents a paradigm shift from the traditional static model of investigation of oxidative biology to the dynamic model of vascular oxidative stress. The investigation of vascular biology and cardiovascular medicine is made possible by the use of tissue engineering, nanotechnology and stem cell research. This is the first textbook to target a wide readership from academia to industry and government agencies in the field of cardiovascular diseases.
This book will cover the cutting-edge developments in molecular and cellular mechanobiology to date. Readers will have a clear understanding of mechanobiology at the molecular and cellular levels, encompassing the mechanosensors, transducers, and transcription. An integrative approach across different scales from molecular sensing to mechanotransduction and gene modulation for physiological regulation of cellular functions will be explored, as well as applications to pathophysiological states in disease. A comprehensive understanding of the roles of physicochemical microenvironment and intracellular responses in determining cellular function in health and disease will also be discussed.
This book presents the latest findings in the field of cardiac mechanobiology in health and disease. Cardiac mechanobiology provides knowledge of all aspects of mechanobiology of the heart. Cardiomyogenesis is discussed as well as the mechanobiology of cardiac remodeling and regeneration. The molecular mechanisms of mechanoperception and mechanotransduction in cardiomyocytes are explained, as well as stretch induced differentiation of cardiomyocytes derived from induced pluripotent stem cells. This volume of the series Cardiac and Vascular Biology complements the volume Vascular Mechanobiology in Physiology and Disease (volume 8) published in this series. The book is aimed at clinicians as well as researchers in cardiovascular biology, bioengineering and biophysics, and also represents an educational resource for young researchers and students in these fields.
An emerging field at the interface of biology and engineering, mechanobiology explores the mechanisms by which cells sense and respond to mechanical signals—and holds great promise in one day unravelling the mysteries of cellular and extracellular matrix mechanics to cure a broad range of diseases. Mechanobiology: Exploitation for Medical Benefit presents a comprehensive overview of principles of mechanobiology, highlighting the extent to which biological tissues are exposed to the mechanical environment, demonstrating the importance of the mechanical environment in living systems, and critically reviewing the latest experimental procedures in this emerging field. Featuring contributions from several top experts in the field, chapters begin with an introduction to fundamental mechanobiological principles; and then proceed to explore the relationship of this extensive force in nature to tissues of musculoskeletal systems, heart and lung vasculature, the kidney glomerulus, and cutaneous tissues. Examples of some current experimental models are presented conveying relevant aspects of mechanobiology, highlighting emerging trends and promising avenues of research in the development of innovative therapies. Timely and important, Mechanobiology: Exploitation for Medical Benefit offers illuminating insights into an emerging field that has the potential to revolutionise our comprehension of appropriate cell biology and the future of biomedical research.
The ESC Textbook of Vascular Biology is a rich and clearly laid-out guide by leading European scientists providing comprehensive information on vascular physiology, disease, and research.
Piezo Channels, Volume 79, the latest volume in the Current Topics in Membranes series provides the necessary membrane research to assist readers in discovering the current state of a particular field and future directions. New chapters in the updated volume include A Tour de Force: The Discovery, Properties, and Function of Piezo Channels, Piezo1 Channels in Vascular Development and the Sensing of Shear Stress, the Origin of the Force: The Force-From-Lipids Principle Applied to Piezo Channels, Genetic Diseases of PIEZO1 and PIEZO2 Dysfunction, and The Structural Basis for Sensing by the Piezo1 Protein. Users of this series will find an up-to-date presentation of the current knowledge in the field of Piezo Channels. - Written by leading experts in the field - Contains original material, both textual and illustrative, that make it a very relevant reference - Presented in a very comprehensive manner - Ideal reference for both researchers in the field and general readers who will find this book to be relevant and up-to-date
Biomechanical forces play a major role in organ development, shape and function. When exceeding the physiological range, however, they may become detrimental for organ structure and function. This is probably best exemplified by the cardiovascular system, with both the heart and blood vessels being continuously exposed to the biomechanical forces exerted by the flow of blood. In the heart, it is the build-up of pressure inside the ventricles that allows the ejection of blood into the pulmonary and systemic circulation. The luminal diameter of the small arteries in both parts of the circulation determines the resistance to flow. Hence it also determines the level of blood pressure in both the pulmonary and systemic circulation and thus the afterload for both ventricles of the heart. A narrowing of the small arteries (e.g. due to an increase in tone) therefore leads to an increase in blood pressure in the affected part of the circulation. This will decrease organ perfusion but increase the afterload for the corresponding ventricle of the heart. Consequently, the affected ventricle must build up more pressure to maintain cardiac output. However, if the rise in blood pressure (pulmonary or arterial hypertension) persists the increase in wall tension can no longer be compensated by active constriction, thereby forcing the ventricle to resort to other means to unload itself. Typically, this is achieved by structural alterations in its wall which becomes thicker (hypertrophy) and stiffer (remodelling of the extracellular matrix). Ultimately, this maladaptive response may lead to dysfunction and eventually failure of the ventricle, which would only be able to eject a significantly smaller amount of blood into circulation. The increase in wall tension has resulted in an increased stretching of the cardiomyocytes as well as non-cardiomyocytes, such as cardiac fibroblasts, which in turn alters both their phenotype and their environment. Research into the mechanobiology of the heart aims to unravel the molecular and cellular mechanisms underlying the physiological response of the heart to load to learn what goes wrong when the heart is faced with sustained pressure overload. This may pave the way to therapeutically interfering with this maladaptive response and thus preventing either the initial hypertrophy or its transition into heart failure. While the heart is mainly subjected to pressure hence stretch as a biomechanical force, the mechanobiology of vascular cells is somewhat more complex. Endothelial cells lining the luminal surface of each blood vessel are continuously subjected to the viscous drag of flowing blood (referred to as fluid shear stress). Fluid shear stress mainly affects the endothelial cells of the small arteries and arterioles, maintaining them in a dormant phenotype. If blood flow is disturbed (e.g. at arterial bifurcations or curvatures) fluid shear stress declines and may give rise to a shift in phenotype of the endothelial cells. A shift from anti-inflammatory to pro-inflammatory in combination with the reduced flow at these sites may enable leukocyte recruitment and diapedesis, which results in a pro-inflammatory response in the vessel wall. Endothelial cells and in particular vascular smooth muscle cells are subjected to another biomechanical force: the blood pressure. Volume-dependent distention of the vessel wall (which can be achieved through an increase in blood flow) results in an increase in wall tension, thereby stretching of the endothelial and smooth muscle cells. Like the cardiomyocytes of the heart, the vascular smooth muscle cells of the small arteries and arterioles try to normalise wall tension by active constriction, which cannot be maintained for long. These cells subsequently undergo hypertrophy or hyperplasia (depending on the size of the blood vessel) and remodel the extracellular matrix so that the vessel wall also becomes thicker and stiffer. This in turn raises their resistance to flow and may contribute to the increase in blood pressure in either the pulmonary or systemic circulation. Research into the mechanobiology of the blood vessels aims to unravel the molecular and cellular mechanisms underlying the physiological response of the vascular cells to pressure (wall tension) and flow (shear stress). It also aims to uncover what goes wrong (e.g. in arteriosclerosis or hypertension) and to eventually specifically interfere with these maladaptive remodelling processes. The aforementioned aspects of cardiovascular mechanobiology along with many more facets of this fascinating, timely and highly clinically relevant field of research are addressed by the original research and review articles within this Research Topic.