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When a striated muscle cell is stimulated, eg by nerve impulses, it is activated from the resting state. It develops contractile force, shortens, and then relengthens to its original dimension when stimulation ceases. The resting muscle, in the absence of any stimulation, is remarkably elastic when stretched and released. More than a century of muscle research has focused on the understanding of the structure and molecular processes which underlie active contraction. The widely accepted sliding filament model states that muscle develops active force by the cyclic attachment and detachment of myosin crossbridges to actin filaments and that muscle shortens when actin filaments are pulled to slide pass thick filaments, without changing the length of either filament (I). Despite major advances in the understanding of the molecular basis of active contraction, surprisingly little is known of how the length of contracted muscle is restored and how resting muscle responds to stretch and compression. It is also unclear how muscle cells manage to control the uniform and precise length of thick and thin filaments in the sarcomere. Recent studies of sarcomere-associated cytoskeletal lattices begin to shed light on both questions (reviewed in 2--7).