| Literature DB >> 34400331 |
Andrew D Baik1, Philip Calafati1, Xiaoli Zhang1, Nina A Aaron1, Antonia Mehra1, Sven Moller-Tank1, Lawrence Miloscio1, Maria Praggastis1, Nicholas Giovannone1, Cheryl Pan1, Yajun Tang1, Susannah Bridges1, Alejo Mujica1, Peter Barbounis1, Jean Yanolatos1, Nicholas Gale1, Ning Li1, Christos A Kyratsous1, Christopher J Schoenherr1, Andrew J Murphy1, Aris N Economides2, Katherine D Cygnar3.
Abstract
Lysosomal diseases are a class of genetic disorders predominantly caused by loss of lysosomal hydrolases, leading to lysosomal and cellular dysfunction. Enzyme replacement therapy (ERT), where recombinant enzyme is given intravenously, internalized by cells, and trafficked to the lysosome, has been applied to treat several lysosomal diseases. However, current ERT regimens do not correct disease phenotypes in all affected organs because the biodistribution of enzyme uptake does not match that of the affected cells that require the enzyme. We present here targeted ERT, an approach that utilizes antibody-enzyme fusion proteins to target the enzyme to specific cell types. The antibody moiety recognizes transmembrane proteins involved in lysosomal trafficking and that are also preferentially expressed in those cells most affected in disease. Using Pompe disease (PD) as an example, we show that targeted ERT is superior to ERT in treating the skeletal muscle phenotypes of PD mice both as a protein replacement therapeutic and as a gene therapy.Entities:
Keywords: enzyme therapy; genetic therapy; glycogen storage disease II; hydrolases; lysosomes; protein transport
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Year: 2021 PMID: 34400331 PMCID: PMC8636175 DOI: 10.1016/j.ymthe.2021.08.020
Source DB: PubMed Journal: Mol Ther ISSN: 1525-0016 Impact factor: 11.454