Facioscapulohumeral Dystrophy: Molecular Basis and Therapeutic Opportunities.
Tessa ArendsDanielle C HammSilvère van der MaarelStephen J TapscottPublished in: Cold Spring Harbor perspectives in biology (2024)
Facioscapulohumeral dystrophy (FSHD) is caused by misexpression of the early embryonic transcription factor Double Homeobox Protein 4 (DUX4) in skeletal muscle. DUX4 is normally expressed at the 4-cell stage of the human embryo and initiates a portion of the first wave of embryonic gene expression that establishes the totipotent cells of the embryo. Following brief expression, the DUX4 locus is suppressed by epigenetic silencing and remains silenced in nearly all somatic cells. Mutations that cause FSHD decrease the efficiency of epigenetic silencing of the DUX4 locus and result in aberrant expression of this transcription factor in skeletal muscles. DUX4 expression in these skeletal muscles reactivates part of the early totipotent program and suppresses the muscle program-resulting in a progressive muscular dystrophy that affects some muscles earlier than others. These advances in understanding the cause of FSHD have led to multiple therapeutic strategies that are now entering clinical trials.
Keyphrases
- muscular dystrophy
- gene expression
- transcription factor
- poor prognosis
- skeletal muscle
- induced apoptosis
- dna methylation
- clinical trial
- binding protein
- cell cycle arrest
- endothelial cells
- quality improvement
- duchenne muscular dystrophy
- insulin resistance
- long non coding rna
- signaling pathway
- single cell
- cell death
- type diabetes
- oxidative stress
- randomized controlled trial
- endoplasmic reticulum stress
- genome wide
- bone marrow
- copy number
- pregnancy outcomes
- pluripotent stem cells
- pi k akt