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Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction

PainSci » bibliography » Roman et al 2021
Tags: DOMS, neat, biology, exercise, self-treatment, treatment, inflammation, pain problems, muscle

One article on PainSci cites Roman 2021: A Deep Dive into Delayed-Onset Muscle Soreness

PainSci notes on Roman 2021:

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Regeneration of skeletal muscle is a highly synchronized process that requires muscle stem cells (satellite cells). We found that localized injuries, as experienced through exercise, activate a myofiber self-repair mechanism that is independent of satellite cells in mice and humans. Mouse muscle injury triggers a signaling cascade involving calcium, Cdc42, and phosphokinase C that attracts myonuclei to the damaged site via microtubules and dynein. These nuclear movements accelerate sarcomere repair and locally deliver messenger RNA (mRNA) for cellular reconstruction. Myofiber self-repair is a cell-autonomous protective mechanism and represents an alternative model for understanding the restoration of muscle architecture in health and disease.

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