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Cardiovascular occlusive diseases, such as myocardial infarction or stroke, are still the major cause of morbidity and mortality worldwide and are, particularly during the SARS-CoV-2 pandemic, drastically increasing. Arteriogenesis, which describes the process of natural arterial bypass growth, is a tissue- and life-saving process, which is given to us by mother nature to compensate for the function of a stenosed coronary or peripheral artery non-invasively. Since our first investigations on the mechanisms of collateral artery growth, more than 20 years ago, a lot of progress has been made, which we aim to make accessible in the current book. We present the available animal models and share information on the used state of the art techniques. We describe how fluid shear stress, the trigger for arteriogenesis, is translated into biochemical signal transduction cascades, and we also highlight the functional role of extracellular RNA and Il10. We address the problematic features of arteriogenesis in patients suffering from diabetes mellitus, and provide an overview of currently available or potentially therapeutic approaches to promote arteriogenesis in patients. We focus on the combination of ultrasound and microbubbles, the permanent occlusion of the internal mammary arteries, and simple exercise training. We believe that we have come much closer to achieving our goal of understanding the mechanisms of arteriogenesis, enabling clinicians to promote collateral artery growth in patients and cure vascular occlusive diseases.

Medicine

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Cardiovascular occlusive diseases, such as myocardial infarction or stroke, are still the major cause of morbidity and mortality worldwide and are, particularly during the SARS-CoV-2 pandemic, drastically increasing. Arteriogenesis, which describes the process of natural arterial bypass growth, is a tissue- and life-saving process, which is given to us by mother nature to compensate for the function of a stenosed coronary or peripheral artery non-invasively. Since our first investigations on the mechanisms of collateral artery growth, more than 20 years ago, a lot of progress has been made, which we aim to make accessible in the current book. We present the available animal models and share information on the used state of the art techniques. We describe how fluid shear stress, the trigger for arteriogenesis, is translated into biochemical signal transduction cascades, and we also highlight the functional role of extracellular RNA and Il10. We address the problematic features of arteriogenesis in patients suffering from diabetes mellitus, and provide an overview of currently available or potentially therapeutic approaches to promote arteriogenesis in patients. We focus on the combination of ultrasound and microbubbles, the permanent occlusion of the internal mammary arteries, and simple exercise training. We believe that we have come much closer to achieving our goal of understanding the mechanisms of arteriogenesis, enabling clinicians to promote collateral artery growth in patients and cure vascular occlusive diseases.

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• Reference Manager
• EndNote
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Cardiovascular occlusive diseases, such as myocardial infarction or stroke, are still the major cause of morbidity and mortality worldwide and are, particularly during the SARS-CoV-2 pandemic, drastically increasing. Arteriogenesis, which describes the process of natural arterial bypass growth, is a tissue- and life-saving process, which is given to us by mother nature to compensate for the function of a stenosed coronary or peripheral artery non-invasively. Since our first investigations on the mechanisms of collateral artery growth, more than 20 years ago, a lot of progress has been made, which we aim to make accessible in the current book. We present the available animal models and share information on the used state of the art techniques. We describe how fluid shear stress, the trigger for arteriogenesis, is translated into biochemical signal transduction cascades, and we also highlight the functional role of extracellular RNA and Il10. We address the problematic features of arteriogenesis in patients suffering from diabetes mellitus, and provide an overview of currently available or potentially therapeutic approaches to promote arteriogenesis in patients. We focus on the combination of ultrasound and microbubbles, the permanent occlusion of the internal mammary arteries, and simple exercise training. We believe that we have come much closer to achieving our goal of understanding the mechanisms of arteriogenesis, enabling clinicians to promote collateral artery growth in patients and cure vascular occlusive diseases.

Medicine

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For many years, arteriogenesis, also called collateral formation, has been regarded as being a beneficial process to restore blood flow to distal tissues in occluded arteries. Therefore, it is frequently referred to in relation to therapeutic angiogenesis. Despite the big clinical potential and the many promising clinical trials on arteriogenesis and therapeutic angiogenesis, the exact molecular mechanisms involved in the multifactorial processes of arteriogenesis are still not completely understood. A better understanding is needed in order to define successful clinical therapies. In this Special Issue, multiple aspects of arteriogenesis and therapeutic angiogenesis will be addressed, ranging from the role of inflammatory processes and immune cells, to growth factors, microRNAs and environmental factors like hypoxia. Therapeutic angiogenesis will also be discussed in relation to the atherosclerosis and intraplaque angiogenesis in hypoxic lesions, as well as specific forms of arteriogenesis in relation to spinal cord blood supply and aorta surgery. The effects of exercise, a frequently prescribed therapy for PAD patients, on arteriogenesis are also discussed. Overall, the papers in this Special Issue on arteriogenesis and therapeutic angiogenesis provide important new insights in the underlying pathophysiological mechanism of these complex processes and may be helpful to define a successful future intervention directed at therapeutic angiogenesis.

Medicine --- factor VII activating protease --- HABP2 --- VEGF --- matrigel --- neo-vascularization --- hind limb ischemia --- angiogenesis --- arteriogenesis --- ERK --- endothelial cells --- inflammation --- macrophages --- atherosclerosis --- pericyte --- rAAV --- capillary --- microRNA --- isomiRs --- epitranscriptome --- neovascularization --- A-to-I editing --- m6A --- RNA modifications --- RNA methylation --- lower extremity arterial disease --- peripheral arterial disease --- blood flow restriction --- activity-based benefits --- training effects --- effect mechanism --- hyperoxygenation --- vein graft disease --- vascular biology --- spinal cord ischemia --- paraplegia --- aortic disease --- TAAA --- collateral network --- paraspinous compartment --- NO --- NOTCH --- innate immunity --- mast cell --- GH and eNOS --- IGF-I --- oxidative stress and arterial inflammation --- vascular homeostasis --- GHAS trial --- collateral artery growth --- SMC proliferation --- potassium channel --- KV1.3 --- KCa3.1 --- FGFR-1 --- Egr-1 --- PDFG-R --- αSM-actin --- TLR2/6 --- femoral artery ligation --- blood flow recovery --- collateral growth --- VHL loss of function --- microRNA-212/132 --- factor VII activating protease --- HABP2 --- VEGF --- matrigel --- neo-vascularization --- hind limb ischemia --- angiogenesis --- arteriogenesis --- ERK --- endothelial cells --- inflammation --- macrophages --- atherosclerosis --- pericyte --- rAAV --- capillary --- microRNA --- isomiRs --- epitranscriptome --- neovascularization --- A-to-I editing --- m6A --- RNA modifications --- RNA methylation --- lower extremity arterial disease --- peripheral arterial disease --- blood flow restriction --- activity-based benefits --- training effects --- effect mechanism --- hyperoxygenation --- vein graft disease --- vascular biology --- spinal cord ischemia --- paraplegia --- aortic disease --- TAAA --- collateral network --- paraspinous compartment --- NO --- NOTCH --- innate immunity --- mast cell --- GH and eNOS --- IGF-I --- oxidative stress and arterial inflammation --- vascular homeostasis --- GHAS trial --- collateral artery growth --- SMC proliferation --- potassium channel --- KV1.3 --- KCa3.1 --- FGFR-1 --- Egr-1 --- PDFG-R --- αSM-actin --- TLR2/6 --- femoral artery ligation --- blood flow recovery --- collateral growth --- VHL loss of function --- microRNA-212/132