<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11</volume><submitter>Liu HC</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Proximal spinal muscular atrophy (SMA), a neurodegenerative disorder that causes infant mortality, has no effective treatment. Sodium vanadate has shown potential for the treatment of SMA; however, vanadate-induced toxicity in vivo remains an obstacle for its clinical application. We evaluated the therapeutic potential of sodium vanadate combined with a vanadium detoxification agent, L-ascorbic acid, in a SMA mouse model.&lt;h4>Methods&lt;/h4>Sodium vanadate (200 μM), L-ascorbic acid (400 μM), or sodium vanadate combined with L-ascorbic acid (combined treatment) were applied to motor neuron-like NSC34 cells and fibroblasts derived from a healthy donor and a type II SMA patient to evaluate the cellular viability and the efficacy of each treatment in vitro. For the in vivo studi</pubmed_abstract><journal>BMC medicine</journal><pagination>38</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3682891</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Sodium vanadate combined with L-ascorbic acid delays disease progression, enhances motor performance, and ameliorates muscle atrophy and weakness in mice with spinal muscular atrophy.</pubmed_title><pmcid>PMC3682891</pmcid><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Ting CH</pubmed_authors><pubmed_authors>Wen HL</pubmed_authors><pubmed_authors>Hsieh-Li HM</pubmed_authors><pubmed_authors>Lin-Chao S</pubmed_authors><pubmed_authors>Tsai LK</pubmed_authors><pubmed_authors>Liu HC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sodium vanadate combined with L-ascorbic acid delays disease progression, enhances motor performance, and ameliorates muscle atrophy and weakness in mice with spinal muscular atrophy.</name><description>&lt;h4>Background&lt;/h4>Proximal spinal muscular atrophy (SMA), a neurodegenerative disorder that causes infant mortality, has no effective treatment. Sodium vanadate has shown potential for the treatment of SMA; however, vanadate-induced toxicity in vivo remains an obstacle for its clinical application. We evaluated the therapeutic potential of sodium vanadate combined with a vanadium detoxification agent, L-ascorbic acid, in a SMA mouse model.&lt;h4>Methods&lt;/h4>Sodium vanadate (200 μM), L-ascorbic acid (400 μM), or sodium vanadate combined with L-ascorbic acid (combined treatment) were applied to motor neuron-like NSC34 cells and fibroblasts derived from a healthy donor and a type II SMA patient to evaluate the cellular viability and the efficacy of each treatment in vitro. For the in vivo studi</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Feb</publication><modification>2025-06-01T12:01:04.092Z</modification><creation>2025-06-01T12:01:04.092Z</creation></dates><accession>S-EPMC3682891</accession><cross_references><pubmed>23409868</pubmed><doi>10.1186/1741-7015-11-38</doi></cross_references></HashMap>