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Updated: Feb 7, 2026

Murine Model of Wound Healing
Published on: May 28, 2013
Targeting Oxidative Stress and Mitochondrial Dysfunction in the Treatment of Impaired Wound Healing: A Systematic
Mariola Cano Sanchez1,2, Steve Lancel3, Eric Boulanger4,5
1Laboratory of Cardiovascular Physiology, Antilles University, P-97200 Fort de France, France. mariola.cano@uvic.cat.
Abstract:
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).
Insights
Reactive oxygen species (ROS) are vital for wound healing, but excessive amounts cause chronic wounds. Mitochondrial-targeted antioxidants, like elamipretide, show promise in treating these non-healing wounds by reducing oxidative damage.
Area of Science:
- Biomedical science
- Cell biology
- Wound healing research
Background:
- Wound healing is a complex biological process involving distinct phases.
- Factors like diabetes, aging, and infection can impair healing, leading to chronic wounds.
- Reactive oxygen species (ROS) play a dual role, essential at low levels but damaging in excess, causing oxidative stress and non-healing wounds.
Purpose of the Study:
- To explore the role of reactive oxygen species (ROS) in wound healing.
- To investigate the potential of antioxidant and anti-inflammatory strategies for chronic wound treatment.
- To highlight mitochondrial-targeted antioxidants, specifically elamipretide, for their therapeutic potential.
Main Methods:
- Review of experimental and clinical studies on wound healing and oxidative stress.
- Analysis of the mechanisms by which ROS influence wound healing phases.
- Examination of the effects of mitochondrial-targeted peptides on cellular signaling pathways.
Main Results:
- Low concentrations of ROS are necessary for microbial defense and cell signaling in wound healing.
- Excessive ROS production or impaired detoxification leads to oxidative damage, a primary cause of chronic non-healing wounds.
- Mitochondrial-targeted antioxidants, such as elamipretide, can mitigate mitochondrial dysfunction and inflammation.
Conclusions:
- Antioxidant and anti-inflammatory strategies are beneficial for non-healing wounds.
- Mitochondrial-targeted peptides like elamipretide offer a promising therapeutic approach.
- Elamipretide may exert its effects by modulating NLRP3 inflammasome, NF-κB, and Nrf2 pathways, addressing key aspects of chronic wound pathology.
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