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Targeting Oxidative Stress and Mitochondrial Dysfunction in the Treatment of Impaired Wound Healing: A Systematic Review

1
Laboratory of Cardiovascular Physiology, Antilles University, P-97200 Fort de France, France
2
Tissue Repair and Regeneration Laboratory (TR2Lab), University of Vic-UCC, Vic P-08500 Barcelone, Spain
3
INSERM U1011-EGID, Institut Pasteur de Lille, Université Lille, CHU Lille, F-59000 Lille, France
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INSERM U995-LIRIC Inflammation Research International Centre, Université Lille, F-59000 Lille, France
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Département de Gériatrie, CHU Lille, F-59000 Lille, France
6
Département de Physiologie, CHU Lille, F-59000 Lille, France
*
Author to whom correspondence should be addressed.
Antioxidants 2018, 7(8), 98; https://doi.org/10.3390/antiox7080098
Received: 17 June 2018 / Revised: 10 July 2018 / Accepted: 20 July 2018 / Published: 24 July 2018
Wound healing is a well-tuned biological process, which is achieved via consecutive and overlapping phases including hemostasis, inflammatory-related events, cell proliferation and tissue remodeling. Several factors can impair wound healing such as oxygenation defects, aging, and stress as well as deleterious health conditions such as infection, diabetes, alcohol overuse, smoking and impaired nutritional status. Growing evidence suggests that reactive oxygen species (ROS) are crucial regulators of several phases of healing processes. ROS are centrally involved in all wound healing processes as low concentrations of ROS generation are required for the fight against invading microorganisms and cell survival signaling. Excessive production of ROS or impaired ROS detoxification causes oxidative damage, which is the main cause of non-healing chronic wounds. In this context, experimental and clinical studies have revealed that antioxidant and anti-inflammatory strategies have proven beneficial in the non-healing state. Among available antioxidant strategies, treatments using mitochondrial-targeted antioxidants are of particular interest. Specifically, mitochondrial-targeted peptides such as elamipretide have the potential to mitigate mitochondrial dysfunction and aberrant inflammatory response through activation of nucleotide-binding oligomerization domain (NOD)-like family receptors, such as the pyrin domain containing 3 (NLRP3) inflammasome, nuclear factor-kappa B (NF-κB) signaling pathway inhibition, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). View Full-Text
Keywords: wound healing; reactive oxygen species; mitochondria; advanced glycation end products; diabetes; inflammation; antioxidants wound healing; reactive oxygen species; mitochondria; advanced glycation end products; diabetes; inflammation; antioxidants
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MDPI and ACS Style

Cano Sanchez, M.; Lancel, S.; Boulanger, E.; Neviere, R. Targeting Oxidative Stress and Mitochondrial Dysfunction in the Treatment of Impaired Wound Healing: A Systematic Review. Antioxidants 2018, 7, 98. https://doi.org/10.3390/antiox7080098

AMA Style

Cano Sanchez M, Lancel S, Boulanger E, Neviere R. Targeting Oxidative Stress and Mitochondrial Dysfunction in the Treatment of Impaired Wound Healing: A Systematic Review. Antioxidants. 2018; 7(8):98. https://doi.org/10.3390/antiox7080098

Chicago/Turabian Style

Cano Sanchez, Mariola; Lancel, Steve; Boulanger, Eric; Neviere, Remi. 2018. "Targeting Oxidative Stress and Mitochondrial Dysfunction in the Treatment of Impaired Wound Healing: A Systematic Review" Antioxidants 7, no. 8: 98. https://doi.org/10.3390/antiox7080098

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