2012, Número 4
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Biotecnol Apl 2012; 29 (4)
Impacto perjudicial del exceso agudo y crónico de glucosa en células involucradas en la cicatrización: fibroblastos, miofibroblastos y células precursoras vasculares
Berlanga-Acosta J, López-Mola E, Garcia-Siverio M, Guillen-Nieto G, Lopez-Saura P, Valdez-Pérez C, Puentes-Madera I, Savigne-Gutierrez W, Álvarez-Duarte H, Miranda-Espinosa N, Mir-Benítez AJ, García DD, Mendoza-Mari Y, Martínez-Espina MD, Garcia-Ojalvo A, Subiros-Martinez N, Herrera-Martínez L
Idioma: Ingles.
Referencias bibliográficas: 131
Paginas: 208-217
Archivo PDF: 284.38 Kb.
RESUMEN
La diabetes mellitus tipo 2 implica desórdenes metabólicos no transmisibles, cuya incidencia va en aumento, con una extensión casi pandémica. Predispone a padecer úlceras en las extremidades inferiores y a su cronicidad, al afectar el proceso de cicatrización. También interfiere la inmunidad innata, lo que favorece la infección de posibles lesiones, y puede conducir a la amputación. La hiperglucemia desencadena los efectores tóxicos que incluyen la inflamación y la producción en exceso de especies reactivas de oxígeno y nitrógeno. Los productos finales altamente glicosilados, que se acumulan sistemáticamente, desarticulan la estructura de células y órganos. La deficiencia en el eje insulínico debilita el anabolismo en las lesiones y predispone a la inflamación. Estos factores convergen y debilitan la proliferación, la migración, el direccionamiento, la secreción y la organización de los fibroblastos y células endoteliales, lo que interfiere en la formación de tejido de granulación útil. El lecho de las heridas puede convertirse en una fuente inflamatoria y procatabólica de citocinas, y constituir un ciclo de perpetuación. La toxicidad diabética provoca daños mitocondriales en los fibroblastos y las células endoteliales, que los hace susceptibles de apoptosis y dificulta la granulación del tejido. También afecta el reclutamiento de las células progenitoras endoteliales, e impide la tubulogénesis. La regeneración del tejido epitelial en las lesiones sigue siendo un desafío clínico que depende de múltiples factores biológicos. Nuevas intervenciones médicas, como la infiltración local intralesional del factor de crecimiento epidérmico recombinante, prometen la reducción de las tasas mundiales de amputación.
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