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Cellular Adaptations to High-Intensity and Sprint Interval Training
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Martin J. MacInnis, Lauren E. Skelly
Capillaries are the site of gas, nutrient, and by-product exchange between muscles and blood. Growth of the capillary network within skeletal muscle (i.e., increased capillarization) provides a greater surface area for exchange and reduces the oxygen diffusion distance. The primary stimuli to increase capillary density in humans, which occurs in response to aerobic training over a period of weeks to months, are mechanical (i.e., shear stress and passive muscle stretch) and metabolic (i.e., muscle contractions). As described by Hellsten and Nyberg (50), capillary growth is regulated by transient changes in the concentration of pro-angiogenic (e.g., vascular endothelial growth factor [VEGF], angiopoietin-2) and anti-angiogenic (e.g., endostatin) compounds elicited by exercise.
Antiangiogenic gene therapy: prospects for human application
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Mori Keisuke, Gehlbach Peter L
a more potent antiangiogenic agent than angiostatin, thrombospondin-1, or endostatin.80 Systemic injection of recombinant PEDF protein is reported to prevent the development of retinal neovascularization in mice with oxygen-induced ischemic retinopathy by promoting apoptosis of vascular endothelial cells.81 PEDF is therefore both an endogenous inhibitor of angiogenesis and a neuroprotective protein.
The Role of Light and Electromagnetic Fields in Maintaining Vascular Health
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Collagen is the most abundant protein in the body, representing approximately 25% of the total protein mass. Collagen forms a scaffold to provide strength, structure, and flexibility to the bones, muscles, skin, and tendons. An important member of the collagen family is collagen XVIII, which is almost always found as a proteoglycan with numerous heparan sulfate attachments [15]. The core protein has a molecular mass of 180 kDa, but an additional mass of 120 kDa is completely attributed to attached heparan sulfate chains. Collagen XVIII is found predominantly in the extracellular matrix of the basal laminae, in the lungs, the skin, the skeletal muscles, kidney tubules and glomeruli, cardiac muscle, blood vessels, and the pia mater, the innermost layer of the membranes surrounding the brain and spinal cord. Endostatin, an anti-angiogenic tumor-suppressing peptide, is identically the C-terminal part of collagen XVIII.
The role of extracellular matrix components in angiogenesis and fibrosis: Possible implication for Systemic Sclerosis
Published in Modern Rheumatology, 2018
Vasiliki Liakouli, Paola Cipriani, Paola Di Benedetto, Piero Ruscitti, Francesco Carubbi, Onorina Berardicurti, Noemi Panzera, Roberto Giacomelli
Collagens, the main structural proteins of the ECM, are known to affect EC survival and vessel formation. The molecules mainly involved in angiogenesis are the type I, IV, XV, and XVIII collagen and it is well known that angiogenesis depends on proper collagens biosynthesis and cross-linking. In SSc, type XVIII collagen and in particular, its anti-angiogenic fragment endostatin, modulates the impaired angiogenesis. Type XVIII collagen is a constituent of the vascular BM, abundantly found along blood vessels in the skin and lungs. Type XVIII collagen is mainly released by activated fibroblasts; after its proteolytic cleavage by the MMPs and cathepsin L, B, and K, thus releasing the anti-angiogenic fragment endostatin that is easily detected in the circulation [9]. The release of endostatin represents a local control mechanism of angiogenesis. Although this mechanism is not yet fully elucidated, it has been shown that endostatin inhibits the proteolytic activation of pro-MMP-2 and the catalytic activities of membrane type 1 MMP, an activator of pro-MMP-2, and MMP-2 [10]. MMPs mediate selective proteolytic degradation of the ECM that is required for migration and invasion of ECs at the onset of angiogenesis [11]. Furthermore, endostatin inhibits vascular endothelial growth factor (VEGF)-induced angiogenesis by blocking EC proliferation and migration [12]. Additionally to the anti-migratory effect, endostatin induces EC apoptosis [13] (Figures 1 and 2).
The association between circulating endostatin levels and incident myocardial infarction
Published in Scandinavian Cardiovascular Journal, 2018
Toralph Ruge, Axel C. Carlsson, Jan-Håkan Jansson, Stefan Söderberg, Anders Larsson, Johan Ärnlöv
The pathophysiological role of increased circulating endostatin is not clear. One hypothesis is that increased circulating endostatin mirrors either an increased level of extra cellular matrix (ECM) remodelling as observed in patients with aortic aneurysms [17] or in patients with malignant diseases [2]. Local ECM remodeling in the heart, initiated for example by hypertension, cardiac stress, valve dysfunction, hypertrophy of the myocardium or by MI per se [18], leads to a substantial pathological deposition of extra cellular matrix proteins in the myocardium and results in cardiac fibrosis [18,19]. Cardiac fibrosis has been suggested to be associated with a reduction in local capillary perfusion leading to tissue hypoxia and a subsequent activation of the angiogenic milieu [20]. Importantly, it has been shown that the expression of endostatin is increased in rat cardiomyocytes exposed to hypoxia [21].
The association between circulating endostatin and a disturbed circadian blood pressure pattern in patients with type 2 diabetes
Published in Blood Pressure, 2018
Jonas Wuopio, Carl Johan Östgren, Toste Länne, Lars Lind, Toralph Ruge, Axel C. Carlsson, Anders Larsson, Fredrik H. Nyström, Johan Ärnlöv
Second, angiogenesis is a complex process regulated by several promoting and inhibiting factors [26]. One of the best-studied pro-angiogenetic factors is Vascular Endothelial Growth Factor (VEGF) which promotes angiogenesis in several ways, [26,27]. Endostatin is a potent inhibitor of VEGF and angiogenesis [28]. For example, VEGF and other known stimulators of angiogenesis were downregulated when exposed to endostatin [28,29]. One possible explanation for the findings in our study is that the disturbed circadian blood pressure-pattern, caused by a disturbed sympathetic outflow, induce vasoconstriction and micro-ischemia in the kidney, heart, and arterial walls. The micro-ischemia favors VEGF-formation, and so, to counteract and balance the angiogenetic properties of VEGF, endostatin is released.