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• W2119028999 abstract "Significance Muscular dystrophies linked to the genetic absence or mutations of dysferlin are currently without a relevant therapy. Dysferlin is thought to mediate membrane repair in skeletal muscle, but its localization and specific functions remain controversial. Here we show that dysferlin is enriched in the transverse tubule membrane of skeletal muscle and demonstrate that, in its absence, mechanical stress leads to calcium-dependent muscle injury. Furthermore, we demonstrate that treatment of dysferlin-deficient muscle with the calcium channel blocker diltiazem reduces in vitro experimental and in vivo contraction-induced muscle damage. As diltiazem is approved for clinical use, our results suggest a potential new therapeutic avenue for patients diagnosed with dysferlinopathies." @default.
• W2119028999 created "2016-06-24" @default.
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• W2119028999 date "2013-12-03" @default.
• W2119028999 modified "2023-10-16" @default.
• W2119028999 title "Dysferlin stabilizes stress-induced Ca ²⁺ signaling in the transverse tubule membrane" @default.
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• W2119028999 doi "https://doi.org/10.1073/pnas.1307960110" @default.
• W2119028999 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3870721" @default.
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