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Rol de la modificación por lactilación en la regulación de la muerte celular lític
Xiaokang Zhang1, Jing Luo1, Zhengrong Zhang2
1The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Frontiers in oncology
|February 12, 2026
Resumen
La lactilación de lisina inducida por L-lactato (KL-la) regula la muerte celular lític (LCD) al influir en la función de las proteínas. La KL-la inhibe contextualmente la LCD en tumores pero la promueve en condiciones no tumorales, impactando la progresión de la enfermedad.
Área de la Ciencia:
- Bioquímica
- Epigenética
- Biología Celular
Sus antecedentes:
- El lactato, tradicionalmente visto como un subproducto metabólico, ahora se reconoce como un regulador epigenético clave.
- La lactilación, una novedosa modificación postraduccional, implica la adición de grupos lactilo a las proteínas, afectando su función.
- La muerte celular lític (LCD) es un proceso inflamatorio crucial implicado en diversas patologías.
Objetivo del estudio:
- Sintetizar los hallazgos recientes sobre la interacción regulatoria entre la lactilación de lisina inducida por L-lactato (KL-la) y la LCD.
- Explorar los roles dependientes del contexto de la KL-la en diferentes entornos de enfermedad.
- Discutir las estrategias terapéuticas dirigidas a las vías del metabolismo del lactato y la KL-la.
Principales métodos:
- Revisión y síntesis de la literatura sobre lactilación y muerte celular.
- Análisis de la evidencia emergente que vincula la KL-la con subtipos específicos de LCD (piropoptosis, ferroptosis, NETosis).
- Examen del doble papel de la KL-la en microambientes tumorales versus no tumorales.
Principales resultados:
- La KL-la modula diversas formas de LCD, influyendo en los resultados de la enfermedad.
- En el microambiente tumoral, la KL-la generalmente inhibe la LCD, promoviendo la supervivencia de las células cancerosas.
- En condiciones no tumorales como la inflamación y la isquemia, la KL-la a menudo exacerba la LCD, provocando daño tisular.
Conclusiones:
- El impacto de la KL-la en la LCD depende en gran medida del contexto, variando significativamente entre patologías tumorales y no tumorales.
- La modulación del metabolismo del lactato y las enzimas de KL-la ofrece posibles vías terapéuticas para modular la LCD.
- Las futuras terapias requieren estrategias de precisión que consideren el contexto patológico, la especificidad celular y las dianas moleculares para la eficacia y la seguridad.
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