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Cited by 212

The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.

C. elegans Epidermal Wounding Induces a Mitochondrial ROS Burst that Promotes Wound Repair

Open access
Xu, Suhong, Chisholm, Andrew D.·2014·Developmental Cell

Abstract

SUMMARY Reactive oxygen species (ROS) such as hydrogen peroxide are generated at wound sites and act as long-range signals in wound healing. The roles of other ROS in wound repair are little explored. Here we reveal a cytoprotective role for mitochondrial ROS (mtROS) in C. elegans skin wound healing. We show that skin wounding causes local production of mtROS superoxide at the wound site. Inhibition of mtROS levels by mitochondrial superoxide-specific antioxidants blocks actin-based wound closure, whereas elevation of mtROS promotes wound closure and enhances survival of mutant animals defective in wound healing. mtROS act downstream of wound-triggered Ca2+ influx. We find that the Mitochondrial Calcium Uniporter MCU-1 is essential for rapid mitochondrial Ca2+ uptake and mtROS production after wounding. mtROS can promote wound closure by local inhibition of Rho GTPase activity via a redox-sensitive motif. These findings delineate a pathway acting via mtROS that promotes cytoskeletal responses in wound healing.

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Metadata

Authors
Xu, S., & Chisholm, A. D.
Venue
Developmental Cell
Publisher
Elsevier BV
Published
2014-10
Volume
31
Issue
1
Pages
48-60
ISSN
1534-5807 (ISSN-L)
OpenAlex
W2087238801
Cited by
212
References
20
FWCI
15.96
Type
journal article
Language
en
Open access
bronze

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Xu, S., & Chisholm, A. D. (2014). C. elegans Epidermal Wounding Induces a Mitochondrial ROS Burst that Promotes Wound Repair. Developmental Cell. https://doi.org/10.1016/j.devcel.2014.08.002

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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