Mitochondrial redox signaling enables repair of injured skeletal muscle cells

Adam Horn, Jack H. Van Der Meulen, Aurelia Defour, Marshall Hogarth, Sen Chandra Sreetama, Aaron Reed, Luana Scheffer, Navdeep S. Chandel, Jyoti K. Jaiswal*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


Strain and physical trauma to mechanically active cells, such as skeletal muscle myofibers, injures their plasma membranes, and mitochondrial function is required for their repair. We found that mitochondrial function was also needed for plasma membrane repair in myoblasts as well as nonmuscle cells, which depended on mitochondrial uptake of calcium through the mitochondrial calcium uniporter (MCU). Calcium uptake transiently increased the mitochondrial production of reactive oxygen species (ROS), which locally activated the guanosine triphosphatase (GTPase) RhoA, triggering F-actin accumulation at the site of injury andfacilitatingmembrane repair.Blockingmitochondrial calcium uptake or ROS production prevented injury-triggered RhoA activation, actin polymerization, and plasmamembrane repair. This repairmechanismwas shared between myoblasts, nonmuscle cells, and mature skeletalmyofibers. Quenching mitochondrial ROS in myofibers during eccentric exercise ex vivo caused increased damage to myofibers, resulting in a greater loss of muscle force. These results suggest a physiological role for mitochondria in plasma membrane repair in injured cells, a role that highlights a beneficial effect of ROS.

Original languageEnglish (US)
Article numbereaaj1978
JournalScience Signaling
Issue number495
StatePublished - Sep 5 2017

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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