Oxidative Stress and Wound Healing Mechanisms

Wound healing proceeds through overlapping phases of haemostasis, inflammation, proliferation and remodelling. At physiological levels, reactive oxygen species (ROS) function as critical signalling mediators to eliminate pathogens, recruit reparative cells and promote angiogenesis. However, an imbalance in favour of ROS accumulation—known as oxidative stress—can inflict damage on proteins, lipids and DNA, prolong the inflammatory phase and impede re-epithelialisation and extracellular matrix deposition. Chronic wounds, particularly those associated with diabetes or ageing, exemplify the consequences of sustained oxidative stress, where antioxidant defences are overwhelmed and mitochondria-driven reactive oxygen production exacerbates tissue injury. Emerging mechanistic insights have highlighted the role of regulated cell-death pathways such as ferroptosis, alongside dysregulation of redox-sensitive transcription factors. Restoration of redox homeostasis through activation of the Nrf2 axis, targeted delivery of enzymatic antioxidants and development of ROS-scavenging biomaterials underpins innovative approaches to accelerate tissue repair and improve clinical outcomes.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Oxidative Stress and Wound Healing Mechanisms publication trend

The graph below shows the total number of articles in oxidative stress and wound healing mechanisms across all publications each year (not limited to Nature Index journals).

Technical terms

Reactive oxygen species (ROS): chemically reactive molecules derived from oxygen that act as signalling mediators but cause cellular damage when in excess.

Oxidative stress: a state in which ROS production exceeds the capacity of antioxidant defences, leading to molecular and cellular injury.

Antioxidants: enzymes or small molecules that neutralise ROS and protect tissues from oxidative damage.

Ferroptosis: iron-dependent regulated cell death driven by lipid peroxidation under conditions of oxidative stress.

Nrf2 pathway: a redox-sensitive transcriptional programme that induces expression of antioxidant and cytoprotective genes.

Autophagosomes: intracellular vesicles that sequester damaged organelles or proteins for degradation, contributing to cellular homeostasis and stress adaptation.

References

1. Autophagosomes Defeat Ferroptosis by Decreasing Generation and Increasing Discharge of Free Fe2+ in Skin Repair Cells to Accelerate Diabetic Wound Healing. Advanced Science (2023).
2. Edaravone-Loaded Alginate-Based Nanocomposite Hydrogel Accelerated Chronic Wound Healing in Diabetic Mice. Marine Drugs (2019).
3. Mitochondria‐Targeted Antioxidant SkQ1 Improves Dermal Wound Healing in Genetically Diabetic Mice. Oxidative Medicine and Cellular Longevity (2017).
4. Procyanidin B2 improves endothelial progenitor cell function and promotes wound healing in diabetic mice via activating Nrf2. Journal of Cellular and Molecular Medicine (2020).