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

William Roman; Helena Pinheiro; Mafalda R. Pimentel; Jessica Segalés; Luis M. Oliveira; Esther García-Domínguez; Mari Carmen Gómez-Cabrera; Antonio L. Serrano; Edgar R. Gomes; Pura Muñoz-Cánoves

doi:10.1126/science.abe5620

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

William Roman, Helena Pinheiro, Mafalda R. Pimentel, Jessica Segalés, Luis M. Oliveira, Esther García-Domínguez, Mari Carmen Gómez-Cabrera, Antonio L. Serrano, Edgar R. Gomes, Pura Muñoz-Cánoves

Research output: Contribution to journal › Article › Research › peer-review

98 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	355-359
Number of pages	5
Journal	Science
Volume	374
Issue number	6565
DOIs	https://doi.org/10.1126/science.abe5620
Publication status	Published - 15 Oct 2021
Externally published	Yes

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title = "Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction",

abstract = "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.",

author = "William Roman and Helena Pinheiro and Pimentel, \{Mafalda R.\} and Jessica Segal{\'e}s and Oliveira, \{Luis M.\} and Esther Garc{\'i}a-Dom{\'i}nguez and G{\'o}mez-Cabrera, \{Mari Carmen\} and Serrano, \{Antonio L.\} and Gomes, \{Edgar R.\} and Pura Mu{\~n}oz-C{\'a}noves",

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doi = "10.1126/science.abe5620",

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AU - Roman, William

AU - Pinheiro, Helena

AU - Pimentel, Mafalda R.

AU - Segalés, Jessica

AU - Oliveira, Luis M.

AU - García-Domínguez, Esther

AU - Gómez-Cabrera, Mari Carmen

AU - Serrano, Antonio L.

AU - Gomes, Edgar R.

AU - Muñoz-Cánoves, Pura

PY - 2021/10/15

Y1 - 2021/10/15

N2 - 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.

AB - 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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M3 - Article

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VL - 374

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JO - Science

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

Abstract

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