Key result
Toll-like receptors (TLRs) are over-active in muscular dystrophies and contribute to chronic inflammation and muscle atrophy, making them potential therapeutic targets to slow disease progression.
Why the study?
The involvement of Toll-like receptor signaling in muscle atrophy observed in muscular dystrophies needed exploration.
Targeting Toll-like receptor signaling pathways (TLR2/4 and TLR7/8/9) may offer a therapeutic strategy to slow disease progression and muscle atrophy in muscular dystrophies.
May implicate TLRs in muscular dystrophy inflammation; leaves open whether targeting them alters progression.
Muscle atrophy is an active process controlled by specific transcriptional programs, in which muscle mass is lost by increased protein degradation and/or decreased protein synthesis. This review explores the involvement of Toll-like receptors (TLRs) in the muscle atrophy as it is observed in muscular dystrophies, disorders characterized by successive bouts of muscle fiber degeneration and regeneration in an attempt to repair contraction-induced damage. TLRs are defense receptors that detect infection and recognize self-molecules released from damaged cells. In muscular dystrophies, these receptors become over-active, and are firmly involved in the sustained chronic inflammation exhibited by the muscle tissue, via their induction of pro-inflammatory cytokine expression. Taming the exaggerated activation of TLR2/4 and TLR7/8/9, and their downstream effectors in particular, comes forward as a therapeutic strategy with potential to slow down disease progression.
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Boél De Paepe (2020) conducted a review in Muscular dystrophies. Toll-like receptors (TLRs) was evaluated. Toll-like receptors (TLRs) are over-active in muscular dystrophies and contribute to chronic inflammation and muscle atrophy, making them potential therapeutic targets to slow disease progression.
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