Table 1.
Effect of Aging on Wound Healing |
Cell/Tissue/Organ Involved | Action | References |
---|---|---|---|
Prolong inflammatory phase | ↑Platelets | ↑Pro-inflammatory cytokines (e.g., PDGF, TGF-β & TGF-α) | [57] |
↓Adhesion molecules | Impairs the monocyte infiltration | [46] | |
↓Macrophage | ↓Granulation tissue formation, angiogenesis, collagen and growth factor synthesis ↓M2, hence prolong inflammation and halt tissue repair |
[46,56] | |
↑Pro-inflammatory cytokines | Activates the COX pathway ↑PGE2 production |
[35,56] | |
↑PGE2 | ↓Fibroblast and collagen synthesis, hence impairs the proliferative phase | [35] | |
Oxidative stress | ↑Reactive oxygen species (ROS) | ↑Tissue damage, lipid peroxidation, promote protein breakdown and DNA damage, hence↑cell apoptosis and senescence | [23,64] |
Inefficient microcirculation | Impaired blood vessels | ↓Inflammatory cells and chemical mediators at injury site Relative hypoperfusion at injury site Hypoxia that causes cell death due to apoptosis and necrosis |
[5,64] |
↑ Increase. ↓ Decrease.