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Research Areas


Angiogenesis is the normal physiological process by which new blood vessels and capillary beds sprout from preexisting vessels, resulting in the creation or expansion of a vascular network within a region of tissue. The construction and maintenance of an architecture of blood vessels functions primarily to provide the hosting tissue, and those cells involved in its structure, with a means for importing those nutrients required for survival and maintenance, and removing unnecessary waste. Consequently, the angiogenic process is a fundamental component of embryonic growth and development, tissue repair and wound healing, the resolution of inflammatory responses, and the onset of neoplasia.  The expansion of a vascular network is a relatively fragile process governed by a delicate balance between stimulatory and inhibitory factors, and is, therefore, highly susceptible to instances of disruptive interference at several levels.  Occurrences of angiogenic perversion can result in pathological angiogenesis, which is characterized by the abnormally rapid and uncontrolled proliferation of blood vessels.  Pathological angiogenesis is critical to the transitioning of a tumor to malignancy, and a contributing factor to a multitude of other diseases, including ischemic chronic wounds, cardiovascular disease, diabetic retinopathy, rheumatoid arthritis, macular degeneration, and psoriasis.  Due to its involvement in such an array of diseases, the ability to manipulate angiogenesis through both natural and synthetic inhibitors and activators represents a promising prospect for the prevention and treatment of diseases characterized by abnormal vascularization. 

View References for PeproTech’s products in Angiogenesis/Cardiovascular Research:

Patterned human microvascular grafts enable rapid vascularization and increase perfusion in infarcted rat hearts

Functional Screening Identifies MicroRNAs as Multi-Cellular Regulators of Heart Failure

iPSC-Derived Endothelial Cells Affect Vascular Function in a Tissue-Engineered Blood Vessel Model of Hutchinson-Gilford Progeria Syndrome 

Hyperbaric oxygen activates visfatin expression and angiogenesis via angiotensin II and JNK pathway in hypoxic human coronary artery endothelial cells 

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