Key result
Skeletal muscle excitation-contraction coupling requires mechanical interaction of four core proteins spanning the triad junction.
Why the study?
To review the evolution of knowledge regarding structures and proteins underlying skeletal muscle excitation-contraction coupling, unanswered questions, and future developments to understand muscle weakness and guide therapies.
Provides a review of the structures and proteins underlying skeletal muscle excitation-contraction coupling and its implications for muscle weakness.
Answers are grounded in this paper and cite their sources.
May guide ECC-targeted therapies for muscle weakness; extends molecular framework but remains hypothesis-generating pending trials.
Mobility in humans and all animals depends on the co-ordinated progress of essential steps linking electrical action potentials along the surface membrane of muscle fibres to the increased cytoplasmic Ca 2+ concentrations that activate the contractile proteins. Excitation–contraction (EC) coupling is the transformation of an electrical signal into a massive release of Ca 2+ from intracellular Ca 2+ stores. We consider the evolution of our knowledge of the structures and proteins that underlie skeletal muscle EC coupling, unanswered questions and future developments that will reveal the fundamental molecular events of the coupling process. The deeper understanding gained with future developments will reveal the molecular basis of muscle weakness related to mutations in EC coupling proteins or result from fatigue and aging. The benefits will flow on to the rational design of therapies to increase muscle strength in the many situations where muscle weakness is related to changes in EC coupling.
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Dulhunty et al. (2026) conducted a review in Skeletal muscle excitation-contraction coupling. Skeletal muscle excitation-contraction coupling relies on the mechanical interaction of four core proteins spanning the triad junction.
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