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Sulfur amino acid supplementation displays therapeutic potential in a C. elegans model of Duchenne muscular dystrophy

Ellwood, Rebecca A.; Slade, Luke; Lewis, Jonathan; Torregrossa, Roberta; Sudevan, Surabhi; Piasecki, Mathew; Whiteman, Matthew; Etheridge, Timothy; Szewczyk, Nathaniel J.


Rebecca A. Ellwood

Luke Slade

Jonathan Lewis

Roberta Torregrossa

Surabhi Sudevan

Matthew Whiteman

Timothy Etheridge

Nathaniel J. Szewczyk


Mutations in the dystrophin gene cause Duchenne muscular dystrophy (DMD), a common muscle disease that manifests with muscle weakness, wasting, and degeneration. An emerging theme in DMD pathophysiology is an intramuscular deficit in the gasotransmitter hydrogen sulfide (H2S). Here we show that the C. elegans DMD model displays reduced levels of H2S and expression of genes required for sulfur metabolism. These reductions can be offset by increasing bioavailability of sulfur containing amino acids (L-methionine, L-homocysteine, L-cysteine, L-glutathione, and L-taurine), augmenting healthspan primarily via improved calcium regulation, mitochondrial structure and delayed muscle cell death. Additionally, we show distinct differences in preservation mechanisms between sulfur amino acid vs H2S administration, despite similarities in required health-preserving pathways. Our results suggest that the H2S deficit in DMD is likely caused by altered sulfur metabolism and that modulation of this pathway may improve DMD muscle health via multiple evolutionarily conserved mechanisms.


Ellwood, R. A., Slade, L., Lewis, J., Torregrossa, R., Sudevan, S., Piasecki, M., …Szewczyk, N. J. (2022). Sulfur amino acid supplementation displays therapeutic potential in a C. elegans model of Duchenne muscular dystrophy. Communications Biology, 5(1), Article 1255.

Journal Article Type Article
Acceptance Date Nov 1, 2022
Online Publication Date Nov 16, 2022
Publication Date Nov 16, 2022
Deposit Date Jan 18, 2023
Publicly Available Date Jan 19, 2023
Journal Communications Biology
Electronic ISSN 2399-3642
Peer Reviewed Peer Reviewed
Volume 5
Issue 1
Article Number 1255
Public URL
Publisher URL


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