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El aminoglicosido induce la translocación de RIPOR2 y la externalización de fosfatidilserina a través de mecanismos

Jinan Li¹, Michelle Yang¹, Bo Zhao^1,2,3

¹Department of Otolaryngology-Head and Neck Surgery, Indiana University School of Medicine, Indianapolis, IN, United States.

Frontiers in cellular neuroscience

|August 22, 2025

Resumen

Los aminoglucósidos causan pérdida auditiva al dañar las células ciliadas cocleares. Este estudio revela que la translocación RIPOR2 inducida por aminoglucósidos y la externalización de fosfatidilserina ocurren de forma independiente, lo que sugiere distintas vías de ototoxicidad.

Área de la Ciencia:

Investigación de la ototoxicidad
Biología celular
Mecanismos moleculares de la pérdida auditiva

Sus antecedentes:

Los aminoglucósidos (AG) son cruciales para el tratamiento de infecciones graves, pero pueden causar pérdida auditiva irreversible.
Los AG inducen la muerte de las células ciliadas cocleares a través de la translocación de RIPOR2 y la externalización de fosfatidilserina (PS).
La relación exacta entre estos dos eventos y el papel del cisplatino en la ototoxicidad no está clara.

Objetivo del estudio:

Investigar si la translocación de RIPOR2 inducida por AG y la externalización de PS son eventos independientes.
Explorar el efecto de la externalización de PS en la translocación de RIPOR2 en las células ciliadas.
Comparar los mecanismos ototóxicos de los AG y el cisplatino en las células ciliadas.

Principales métodos:

Tratamiento de células ciliadas de tipo salvaje con AG en diferentes momentos.
Investigación de la localización de RIPOR2 y la externalización de PS.
Evaluación de los efectos del cisplatino en la externalización de PS y la localización de RIPOR2.

Principales resultados:

Las AG desencadenan la translocación de RIPOR2 y la externalización de PS a través de vías moleculares independientes.
La externalización de PS no parece influir en la translocación RIPOR2 inducida por AG.
El cisplatino y los AG inducen la muerte de las células ciliadas a través de vías moleculares distintas, a pesar de las características ototóxicas compartidas.

Conclusiones:

La ototoxicidad inducida por AG implica vías moleculares paralelas para la translocación de RIPOR2 y la externalización de PS.
El cisplatino y los AG representan mecanismos distintos de daño de las células ciliadas.
La comprensión de estas vías distintas puede informar estrategias para mitigar la pérdida auditiva inducida por medicamentos.

Palabras clave:

El RIPOR2 Aminoácidos y sus derivados célula capilar Transducción mecánica Ototoxicidad Fósfatidilserina y sus derivados

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