title: The role of endoglin in post-ischemic revascularization.
abstract: Following arterial occlusion, blood vessels respond by forming a new network of functional capillaries (angiogenesis), by reorganizing preexisting capillaries through the recruitment of smooth muscle cells to generate new arteries (arteriogenesis) and by growing and remodeling preexisting collateral arterioles into physiologically relevant arteries (collateral development). All these processes result in the recovery of organ perfusion. The importance of endoglin in post-occlusion reperfusion is sustained by several observations: (1) endoglin expression is increased in vessels showing active angiogenesis/remodeling; (2) genetic endoglin haploinsufficiency in humans causes deficient angiogenesis; and (3) the reduction of endoglin expression by gene disruption or the administration of endoglin-neutralizing antibodies reduces angiogenesis and revascularization. However, the precise role of endoglin in the several processes associated with revascularization has not been completely elucidated and, in some cases, the function ascribed to endoglin by different authors is controversial. The purpose of this review is to organize in a critical way the information available for the role of endoglin in several phenomena (angiogenesis, arteriogenesis and collateral development) associated with post-ischemic revascularization.
authors.affiliation: Renal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, Salamanca, Spain.|Biomedical Research Institute of Salamanca (IBSAL), Salamanca, Spain.
authors.forename: Elena
authors.initials: E
authors.lastname: Núñez-Gómez
authors.affiliation: Renal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, Salamanca, Spain.|Biomedical Research Institute of Salamanca (IBSAL), Salamanca, Spain.
authors.forename: Miguel
authors.initials: M
authors.lastname: Pericacho
authors.affiliation: Renal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, Salamanca, Spain.|Biomedical Research Institute of Salamanca (IBSAL), Salamanca, Spain.
authors.forename: Claudia
authors.initials: C
authors.lastname: Ollauri-Ibáñez
authors.affiliation: Centro de Investigaciones Biológicas, Spanish National Research Council (CIB, CSIC), Madrid, Spain.|Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Madrid, Spain.
authors.forename: Carmelo
authors.initials: C
authors.lastname: Bernabéu
authors.affiliation: Renal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, Salamanca, Spain. jmlnovoa@usal.es.|Biomedical Research Institute of Salamanca (IBSAL), Salamanca, Spain. jmlnovoa@usal.es.
authors.forename: José M
authors.initials: JM
authors.lastname: López-Novoa
mesh_terms: D000818:Animals; D000071063:Endoglin / Q000378:metabolism*; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007511:Ischemia / Q000378:metabolism* / Q000503:physiopathology*; D018919:Neovascularization, Physiologic; D015398:Signal Transduction; D066253:Vascular Remodeling
chemical_list: D000071063:Endoglin
keywords: Angiogenesis; Arterial occlusion; Arteriogenesis; Collateral growth; Endoglin; Ischemia; Revascularization; Vascular remodeling