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Sample Preparation to Bioinformatics Analysis of DNA Methylation: Association Strategy for Obesity and Related Trait Studies
Published on: May 6, 2022
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Los antecedentes de obesidad desencadenan cambios epigenéticos persistentes en la inmunidad innata y exacerban la
Masayuki Hata1,2, Elisabeth M M A Andriessen3, Maki Hata1
1Department of Ophthalmology, Maisonneuve-Rosemont Hospital Research Centre, University of Montreal, Montreal, Quebec H1T 2M4, Canada.
Science (New York, N.Y.)
|January 5, 2023
Resumen
La obesidad pasada reprograma el sistema inmunológico, lo que lleva a la neuroinflamación y la pérdida de visión incluso después de la normalización del peso. Esta memoria inmune contribuye a la degeneración macular relacionada con la edad y otras enfermedades relacionadas con el envejecimiento.
Área de la Ciencia:
- Inmunología
- La neurociencia
- Oftalmología
Sus antecedentes:
- La degeneración macular relacionada con la edad (AMD) es una de las principales causas de ceguera, vinculada a la neuroinflamación y factores como la obesidad.
- Las condiciones de salud crónicas pueden tener impactos duraderos debido a los efectos acumulativos de la esperanza de vida.
Objetivo del estudio:
- Investigar cómo la obesidad inducida por la dieta temprana afecta el sistema inmunológico innato y predispone a la neuroinflamación y la pérdida de la visión.
- Identificar los mecanismos moleculares que vinculan la obesidad a la patogénesis de la DMAE.
Principales métodos:
- Estudió los efectos a largo plazo de la obesidad inducida por la dieta en el sistema inmunológico innato en un modelo relevante para las enfermedades del envejecimiento.
- Los cambios moleculares analizados en las células mieloides, incluyendo la remodelación de la cromatina y los cambios metabólicos.
- Se evaluó el impacto en la patología de la retina, incluida la angiogénesis y la degeneración neuronal.
Principales resultados:
- La obesidad en la vida temprana indujo una reprogramación persistente del sistema inmunológico, incluso después de la normalización metabólica.
- El ácido esteárico, a través del receptor tipo Toll 4 (TLR4), alteró la unión de la cromatina y AP-1, promoviendo la inflamación.
- Las células mieloides pasaron de la fosforilación oxidativa a la glucólisis, aumentando la transcripción de citoquinas proinflamatorias.
- Esta reprogramación exacerbó la angiogénesis retiniana y la degeneración neuronal, lo que condujo a la pérdida de la visión.
Conclusiones:
- Un historial de obesidad puede alterar permanentemente la función de las células inmunes, predisponer a las personas a afecciones neuroinflamatorias como la DMAE.
- Comprender estos cambios inmunológicos a largo plazo es crucial para desarrollar estrategias para prevenir o tratar la pérdida de visión relacionada con la edad.
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