ABSTRACT
Connective tissue growth factor (CTGF) is increased in several pathologies associated with fibrosis, including multiple renal diseases. CTGF is involved in biological processes such as cell cycle regulation, migration, adhesion and angiogenesis. Its expression is regulated by various factors involved in renal damage, such as transforming growth factor- , Angiotensin II, high concentrations of glucose and cellular stress. CTGF is involved in the initiation and progression of renal damage to be able to induce an inflammatory response and promote fibrosis, identified as a potential therapeutic target in the treatment of kidney diseases. In this paper we review the main actions of CTGF in renal disease, the intracellular action mechanisms and therapeutic strategies for its blocking.
Subject(s)
Connective Tissue Growth Factor/physiology , Kidney Diseases/etiology , Disease Progression , HumansABSTRACT
El factor de crecimiento de tejido conectivo (CTGF) aparece aumentado en diferentes patologías asociadas a fibrosis, incluidas múltiples enfermedades renales. CTGF participa en procesos biológicos, como la regulación del ciclo celular, migración, adhesión y angiogénesis. Su expresión está regulada por diversos factores implicados en el daño renal, entre los que destacan el factor la angiotensina II, el factor de crecimiento transformante-beta, altas concentraciones de glucosa y situaciones de estres celular. CTGF participa en el inicio y progresión del daño renal al ser capaz de inducir una respuesta inflamatoria y promover la fibrosis, señalándole como una posible diana terapéutica en el tratamiento de patologías renales. En este trabajo revisamos las principales acciones de CTGF en la patología renal, los mecanismos intracelulares de actuación y las estrategias terapéuticas para su bloqueo (AU)
Connective tissue growth factor (CTGF) is increased in several pathologies associated with fibrosis, including multiple renal diseases. CTGF is involved in biological processes such as cell cycle regulation, migration, adhesion and angiogenesis. Its expression is regulated by various factors involved in renal damage, such as Angiotensin II, transforming growth factor-beta, high concentrations of glucose and cellular stress. CTGF is involved in the initiation and progression of renal damage to be able to induce an inflammatory response and promote fibrosis, identified as a potential therapeutic target in the treatment of kidney diseases. In this paper we review the main actions of CTGF in renal disease, the intracellular action mechanisms and therapeutic strategies for its blocking (AU)
Subject(s)
Humans , Intercellular Signaling Peptides and Proteins , Transforming Growth Factor beta/physiology , Renal Insufficiency, Chronic/physiopathology , Connective Tissue Cells/pathology , Fibrosis/physiopathology , Neovascularization, Physiologic/physiology , Cell Cycle/physiology , Inflammation/physiopathologyABSTRACT
Los estudios realizados en biopsias peritoneales de pacientes con fallo renal que son tratados mediante diálisis peritoneal (DP) han demostrado que esta terapia provoca daños en la membrana peritoneal, caracterizados por fibrosisy angiogénesis, y que culminan en la pérdida de la capacidad de ultrafiltración de la membrana peritoneal. Estos estudios son descriptivos y apenas han contribuido al conocimiento de los mecanismos implicados en el proceso patológico inducido por la exposición de la membrana peritoneal a los líquidos de diálisis. Así, es necesario el desarrollo de modelos experimentales en animales para suplirlas deficiencias presentadas por los estudios en pacientes. Aquí tratamos las ventajas y dificultades de la utilización de modelos experimentales de diálisis peritoneal y las expectativas para el futuro (AU)
The studies performed with human peritoneal biopsies of peritonealdialysis-patients have demonstrated that exposure to peritonealdialysis fluid induce peritoneal deterioration. The main alterations of peritoneal membrane are fibrosis and angiogenesis that ends with the failure of the ultrafiltration capacity of the peritonealmembrane. These studies are descriptivist and scarcely help to investigate the mechanisms and stages involved on the process. Therefore, it is necessary to supply the deficiencies presented by the studies with patients. The experimental models have strongly contributed to the knowledge of the pathologic process that is induced by the continuous exposition of the peritonealmembrane to the dialysis fluids. Most of the peritonealdialysis studies use the rat as the experimental animal. Due to the difficulty of working with small animals, few studies have been done in mice. However, models in mice offers great advantages,as long as they allow us to employ different strains and genetically modified animals. We have recently developed an experimenta lmodel in mouse of exposure of the peritoneal membrane to dialysis fluids, which resembles the process of peritonealdamage that take place during peritoneal dialysis treatment inhuman patients (AU)
Subject(s)
Animals , Peritoneal Dialysis/methods , Renal Insufficiency/therapy , Epithelium/injuries , Disease Models, Animal , Ultrafiltration , Dialysis Solutions/adverse effectsABSTRACT
The studies performed with human peritoneal biopsies of peritoneal dialysis -patients have demonstrated that exposure to peritoneal dialysis fluid induce peritoneal deterioration. The main alterations of peritoneal membrane are fibrosis and angiogenesis that ends with the failure of the ultrafiltration capacity of the peritoneal membrane. These studies are descriptivist and scarcely help to investigate the mechanisms and stages involved on the process. Therefore, it is necessary to supply the deficiencies presented by the studies with patients. The experimental models have strongly contributed to the knowledge of the pathologic process that is induced by the continuous exposition of the peritoneal membrane to the dialysis fluids. Most of the peritoneal dialysis studies use the rat as the experimental animal. Due to the difficulty of working with small animals, few studies have been done in mice. However, models in mice offers great advantages, as long as they allow us to employ different strains and genetically modified animals. We have recently developed an experimental model in mouse of exposure of the peritoneal membrane to dialysis fluids, which resembles the process of peritoneal damage that take place during peritoneal dialysis treatment in human patients.
