Pompe Disease and Autophagy: Partners in Crime, or Cause and Consequence?

M. Rodriguez-Arribas, J. M. Bravo-San Pedro, R. Gomez-Sanchez, S. M. S. Yakhine-Diop, G. Martinez-Chacon, E. Uribe-Carretero, D. C. J. Pinheiro De Castro, I. Casado-Naranjo, A. Lopez de Munain, M. Niso-Santano, J. M. Fuentes, R. A. Gonzalez-Polo

    Research output: Contribution to journalReview articlepeer-review

    7 Citations (Scopus)

    Abstract

    Pompe disease or glycogen storage disease type II (OMIM: 232300) is a lysosomal storage disorder resulting from a partial or total lack of acid alphaglucosidase, which may produce muscle weakness, gait abnormalities, or even death by respiratory failure. In the last decade, autophagy has been proposed as a mechanism involved in the severity of symptoms related to this disorder and as a potential therapeutic target to alleviate disease progression. This review summarizes the relationship between autophagy and Pompe disease, including what information has been recently discovered and what remains unclear.

    Original languageEnglish
    Pages (from-to)2275-2285
    Number of pages11
    JournalCURRENT MEDICINAL CHEMISTRY
    Volume23
    Issue number21
    DOIs
    Publication statusPublished - 2016

    Keywords

    • Autophagy
    • Glycogen synthase
    • LC3
    • Lysosomes
    • Pompe disease
    • Recombinant human GAA
    • ACID ALPHA-GLUCOSIDASE
    • ENZYME REPLACEMENT THERAPY
    • SKELETAL-MUSCLE
    • LATE-ONSET
    • MITOCHONDRIAL DYSFUNCTION
    • MONITORING AUTOPHAGY
    • OXIDATIVE STRESS
    • GENE-THERAPY
    • CELL-DEATH
    • SUPPRESSION

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