A molecular perspective on diabetic wound healing: Exploring key signaling pathways

Area of Science:

• Biomedical Science
• Molecular Biology
• Wound Healing Research

Background:

• Diabetic wounds affect 25% of diabetics globally, with delayed healing due to hyperglycemia, oxidative stress, and inflammation.
• These factors disrupt essential tissue repair processes, leading to chronic non-healing wounds.

Purpose of the Study:

• To review molecular signaling pathways critical for diabetic wound healing.
• To discuss novel therapeutic strategies targeting these pathways for improved patient outcomes.

Main Methods:

• Analysis of key signaling pathways including Wnt/β-catenin, MAPK/ERK, NF-κB/NLRP3, Hippo-YAP, HIF-1α/VEGF-SDF-1α, AKT/eNOS, PI3K/Akt, Nrf2, TGF-β/Smad, and Notch.
• Examination of how diabetes-associated factors (AGEs, ROS, inflammation) disrupt these pathways.
• Review of emerging therapies such as nanoparticle-based treatments, exosome therapies, and bioactive compounds.

Main Results:

• Diabetes disrupts multiple signaling pathways, impairing keratinocyte migration, angiogenesis, and extracellular matrix remodeling.
• These pathways regulate crucial aspects of healing: cell growth, blood vessel formation, inflammation control, and tissue repair.
• Emerging therapies show promise by targeting these disrupted pathways.

Conclusions:

• Therapeutic strategies should target multiple interacting pathways for effective diabetic wound management, rather than single components.
• Future approaches may involve personalized medicine, AI diagnostics, and combination therapies for chronic diabetic wounds.