Функции митохондрий в механизмах активации тромбоцитов : модель участия митохондриально-ассоциированных мембран
Ключевые слова:
тромбоциты, гемостаз, митохондрии, митохондриально-ассоциированные мембраны (МАМs), кальциевая сигнализация, апоптоз, рак, сахарный диабет, ишемическая болезнь сердца, болезнь АльцгеймераАннотация
В статье представлены современные данные о молекулярных механизмах функционирования тромбоцитов и роли в этом процессе митохондрий и митохондриально-ассоциированных мембран, а также проведен анализ возможных механизмов участия митохондриально-ассоциированных мембран тромбоцитов в развитии ряда патологических состояний человека неинфекционной природы.
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Gutierrez T., Parra V., Troncoso R., Pennanen C., Contreras-Ferrat A., Vasquez-Trincado C., Morales P.E., Lopez-Crisosto C., Sotomayor-Flores C., Chiong M., Rothermel B.A., Lavandero S. Alteration in mitochondrial Ca2+ uptake disrupts insulin signaling in hypertrophic cardiomyocytes. Cell Commun. Signal. 2014, vol. 12, pp. 68-81.
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Tanaka T., Kutomi G., Kajiwara T., Kukita K., Kochin V., Kanaseki T. Cancer-associated oxidoreductase ERO1-alpha promotes immune escape through up-regulation of PD-L1 in human breast cancer. Oncotarget. 2017, vol. 8, no. 15, pp. 24706-24718.
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Cheung K-H.H., Shineman D., Müller M., Cárdenas C., Mei L., Yang J., Tomita T., Iwatsubo T., Lee V.M., Foskett J.K. Mechanism of Ca2+ disruption in Alzheimer’s disease by presenilin regulation of InsP3 receptor channel gating. Neuron. 2008, vol. 58, pp. 871-883.
