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El factor de transcripción ZEB2 es esencial para la diferenciación de las células del músculo liso ureteral
Sudhir Kumar1, Xueping Fan1, Harshita Pattam1
1Nephrology Section, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston Medical Center, Boston, Massachusetts, United States of America.
PLoS genetics
|January 23, 2026
Resumen
El síndrome de Mowat-Wilson (MWS) involucra el gen ZEB2. Este estudio encontró que ZEB2 es esencial para el desarrollo de las células del músculo liso ureteral, lo que explica los defectos del tracto urinario en pacientes con MWS.
Área de la Ciencia:
- Biología del Desarrollo
- Genética
- Urología
Sus antecedentes:
- El síndrome de Mowat-Wilson (MWS) es un trastorno genético relacionado con mutaciones en el gen ZEB2.
- Se observan anomalías congénitas del riñón y del tracto urinario (CAKUT) en pacientes con MWS.
- El papel específico de ZEB2 en el desarrollo del tracto urinario no se comprende bien.
Objetivo del estudio:
- Investigar el papel del gen ZEB2 en el desarrollo del uréter del ratón.
- Elucidar los mecanismos celulares y moleculares detrás de CAKUT en MWS.
Principales métodos:
- Se examinó la expresión de ZEB2 en los uréteres del ratón en desarrollo.
- Se generaron ratones knockout condicionales específicos del mesénquima ureteral Zeb2 (Zeb2 cKO).
- Se analizó la morfología y la histología del tracto urinario en ratones Zeb2 cKO y de tipo salvaje.
Principales resultados:
- ZEB2 se expresa en las células mesenquimales ureterales durante el desarrollo.
- La deleción de Zeb2 en estas células provocó hidrouréter e hidronefrosis (uroptía obstructiva).
- Se observó ausencia de la capa de músculo liso y expansión de la túnica adventicia en ratones Zeb2 cKO.
Conclusiones:
- ZEB2 es fundamental para la diferenciación normal de las células del músculo liso ureteral.
- El desarrollo anormal del músculo liso ureteral debido a la disfunción de ZEB2 probablemente contribuye a CAKUT en MWS.
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