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Journal ArticleDOI

The molecular control of angiogenesis

Oliver Distler, +1 more
- 01 Jan 2002 - 
- Vol. 21, Iss: 1, pp 33-49
TLDR
The rapid increase in the knowledge about the molecular mechanisms of angiogenesis has led to first treatment trials in diseases with both enhanced and reduced angiogeneis, and although initial results are promising, much more work has to be done to consdier anti-angiogenic or pro-angIogenic approaches as reliable therapeutic tools.
Abstract
Angiogenesis is a key event in a broad range of pathological conditions including both diseases with an enhanced and insufficient angiogenesis. Angiogenesis is often initiated with vasodilation accompanied by an increase in vascular permeability. After destabilization of the vessel wall and degradation of the surrounding extracellular matrix, extravasation of plasma proteins provides a provisional scaffold for the migration of endothelial cells. Endothelial cell proliferation and migration themselves are under tight control by a balance of angiogenesis inducers and inhibitors. A large number of angiogenic factors work together in a highly coordinated manner to induce endothelial cell outgrowth and the formation of functional vessels. On the other hand, angiostatic factors may play a critical role in the pathogenesis of ischemic diseases and contribute to the termination of physiological angiogenesis. Angiogenesis ends with the recruitment of pericytes and smooth muscle cells, which stabilize the newly formed vessel. The rapid increase in the knowledge about the molecular mechanisms of angiogenesis has led to first treatment trials in diseases with both enhanced and reduced angiogenesis. Although initial results are promising, much more work has to be done to consider anti-angiogenic or pro-angiogenic approaches as reliable therapeutic tools.

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Citations
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Journal ArticleDOI

Pericytes: Pluripotent Cells of the Blood Brain Barrier

TL;DR: Evidence that pericytes are stem cells derived from historical work and from more recent literature is considered, and a number of misconceptions about the pericyte are attempted to dispel that has lead to confusion in the literature.
Journal ArticleDOI

Elastin-derived peptides enhance angiogenesis by promoting endothelial cell migration and tubulogenesis through upregulation of MT1-MMP.

TL;DR: Batimastat, an inhibitor of furin convertase and timP-2, but not TIMP-1, totally abolished the influence of elastin-derived peptides (EDPs) on cell migration and tubulogenesis, thus favoring the involvement of MT1-MMP in such processes.
Journal ArticleDOI

Role of hyaluronan in angiogenesis and its utility to angiogenic tissue engineering.

TL;DR: The role and significance of hyaluronan (HA), a glycosaminoglycan (GAG) component of connective tissues, in physiologic and pathologicalAngiogenesis, its applicability as a therapeutic to stimulate or suppress angiogenesis in situ within necrotic tissues in vivo, and the factors determining its potential utility as a pro-angiogenic stimulus that will enable tissue engineering of neo-vascularized and functional tissue constructs for clinical use are provided.
Journal ArticleDOI

Human α1 type IV collagen NC1 domain exhibits distinct antiangiogenic activity mediated by α1β1 integrin

TL;DR: It is demonstrated that human α1(IV)NC1 binds to α1β1 integrin, competes with type IV collagen binding to α 1β1Integrin, and inhibits migration, proliferation, and tube formation by ECs, and suggests a critical role for integrins in Hypoxia and hypoxia-induced angiogenesis.
References
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Journal ArticleDOI

Angiogenesis in cancer and other diseases

TL;DR: Pathological angiogenesis is a hallmark of cancer and various ischaemic and inflammatory diseases and integrated understanding is leading to the development of a number of exciting and bold approaches to treat cancer and other diseases, but owing to several unanswered questions, caution is needed.
Journal ArticleDOI

Endostatin: an endogenous inhibitor of angiogenesis and tumor growth.

TL;DR: This work has identified endostatin, an angiogenesis inhibitor produced by hemangioendothelioma, a 20 kDa C-terminal fragment of collagen XVIII that specifically inhibits endothelial proliferation and potently inhibitsAngiogenesis and tumor growth.
Journal ArticleDOI

Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele

TL;DR: It is reported that formation of blood vessels was abnormal, but not abolished, in heterozygous VEGF-deficient (VEGF+/-) embryos, generated by aggregation of embryonic stem (ES) cells with tetraploid embryos (T-ES)16,17, and even more impaired in homozygous D1-VEGF- deficient (VDGF-/-) T-ES embryos, resulting in death at mid-gestation.
Journal ArticleDOI

Mechanisms of angiogenesis and arteriogenesis.

TL;DR: The cellular and molecular mechanisms underlying the formation of endothelium-lined channels and their maturation via recruitment of smooth muscle cells (arteriogenesis) during physiological and pathological conditions are summarized, alongside with possible therapeutic applications.
Journal ArticleDOI

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TL;DR: The generation of mice deficient in Flk-1 by disruption of the gene using homologous recombination in embryonic stem (ES) cells is reported, indicating that FlK-1 is essential for yolk-sac blood-island formation and vasculogenesis in the mouse embryo.
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Although initial results are promising, much more work has to be done to consdier anti-angiogenic or pro-angiogenic approaches as reliable therapeutic tools.