Regulator of Angiogenesis and Vascular Function: A 2019 Update of the Vasoinhibin Nomenclature
Por:
Triebel, Jakob, Pablo Robles, Juan, Zamora, Magdalena, Martinez de la Escalera, Gonzalo, Bertsch, Thomas, Clapp, Carmen
Publicada:
10 abr 2019
Categoría:
Endocrinology, diabetes and metabolism
Resumen:
Proteolytic cleavage of prolactin (PRL), the human anterior pituitary hormone fundamental for lactation can generate vasoinhibin, a peptide-hormone with endocrine, paracrine, and autocrine effects not shared with its precursor. Vasoinhibin effects include the regulation of blood vessel growth, permeability, and dilation (1, 2), and non-vascular effects such as stimulation of vasopressin release (3), thrombolytic actions (4), inhibition of neurite outgrowth (5), and the stimulation of anxiety- and depression-related behaviors (6). Vasoinhibin signals through a still-unidentified receptor on endothelial cells distinct from the PRL-receptor and interacts with multiple binding partners (4, 7, 8). The role of vasoinhibin in biology and disease is evolving and its understanding requires the revision of its nomenclature, which is the purpose of this commentary (9). The regulation of vasoinhibin generation occurs at the hypothalamo, the pituitary, and the target tissue levels and this organizational principle is described as the prolactin/vasoinhibin axis (10). A dysregulation of this axis is relevant in several diseases. Recent studies have focused on retinal disorders (11, 12), joint diseases (13), and pregnancy associated syndromes, for example diabetic retinopathy (11, 14), rheumatoid arthritis (13), peripartum-cardiomyopathy (15), and pre-eclampsia (16, 17). Two clinical trials in which vasoinhibin levels are the target of pharmacological interventions were initiated, one for the treatment of diabetic retinopathy and diabetic macular edema, and another for the treatment of peripartum cardiomyopathy (18, 19). The principles and rationales behind these clinical trials were recently reviewed (20). Landmark studies on the physiological and pathophysiological effects of vasoinhibin are presented in Table 1. © 2019 Triebel, Robles, Zamora, Martínez de la Escalera, Bertsch and Clapp.
Filiaciones:
Triebel, Jakob:
Gen Hosp Nuremberg, Inst Clin Chem Lab Med & Transfus Med, Nurnberg, Germany
Paracelsus Med Univ Nuremberg, Nurnberg, Germany
Institute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine, General Hospital Nuremberg and Paracelsus Medical University Nuremberg, Nuremberg, Germany
Pablo Robles, Juan:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Queretaro, Mexico
Zamora, Magdalena:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Queretaro, Mexico
Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico
Martinez de la Escalera, Gonzalo:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Queretaro, Mexico
Bertsch, Thomas:
Gen Hosp Nuremberg, Inst Clin Chem Lab Med & Transfus Med, Nurnberg, Germany
Paracelsus Med Univ Nuremberg, Nurnberg, Germany
Institute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine, General Hospital Nuremberg and Paracelsus Medical University Nuremberg, Nuremberg, Germany
Clapp, Carmen:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Queretaro, Mexico
Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico
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