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This review was written with the aim of examining the effects that cause an insult, such as a wound, to an organ, such as the skin. Before examining the cellular mechanisms relating to wound healing, the reader is invited to read about the structure of the skin as a necessary basis for understanding the final aim of this review. The structure of the skin as a basis for understanding the phenomena relating to wound healing is addressed, taking into account the updated literature that addresses the numerous problems of the skin microenvironment. Starting from this awareness, the paragraphs dedicated to wound healing become complicated when this phenomenon is not implemented and therefore while the problems of chronic wounds, keloids, and hypertrophic scars are addressed, these are pathologies that are still difficult to understand and treat today.
This review was written with the aim of examining the effects that cause an insult, such as a wound, to an organ, such as the skin. Before examining the cellular mechanisms relating to wound healing, the reader is invited to read about the structure of the skin as a necessary basis for understanding the final aim of this review. The structure of the skin as a basis for understanding the phenomena relating to wound healing is addressed, taking into account the updated literature that addresses the numerous problems of the skin microenvironment. Starting from this awareness, the paragraphs dedicated to wound healing become complicated when this phenomenon is not implemented and therefore while the problems of chronic wounds, keloids, and hypertrophic scars are addressed, these are pathologies that are still difficult to understand and treat today.
Wound healing is a complex biological process that can lead to chronic wounds, keloids, and hypertrophic scars when disrupted. Chronic wounds result from a prolonged inflammatory phase and impaired re-epithelialization. Keloids are characterized by excessive collagen deposition beyond the original wound boundaries, driven by persistent inflammation and fibroblast hyperactivity. Hypertrophic scars, on the other hand, are confined to the wound edges and are caused by an imbalance in collagen synthesis and degradation, typically resolving over time. The therapeutic approach to wound healing impairment involves a range of strategies, including non-invasive (which focus on supporting the natural healing process), minimally invasive, and aggressive interventions (such as surgical approach, often reserved for severe or refractory cases). Emerging therapies, including stem cell treatments and botulinum toxin injections, offer new hope for improving outcomes in patients with wound healing impairments. This review highlights the distinct mechanisms underlying chronic wounds, keloids, and hypertrophic scars and discusses their respective therapeutic approaches, focusing on both established and emerging therapies. Understanding these mechanisms is crucial for optimizing treatment strategies and improving patient outcomes.
Background/Objectives: Photodynamic therapy (PDT) is widely utilized in dermatology for the treatment of various skin conditions. Despite its effectiveness, the exact biomolecular changes underlying therapeutic outcomes remain only partially understood. This review, through a transversal approach, aims to provide an in-depth exploration of molecular biomarkers involved in PDT, evaluate its underlying mechanisms, and examine how these insights can contribute to enhanced treatment protocols and personalized therapy approaches. Methods: A narrative review of the literature was conducted, targeting peer-reviewed articles and clinical trials that focus on PDT and its molecular biomarker effects on dermatological conditions. The databases searched included PubMed, Scopus, and Web of Science, and the inclusion criteria encompassed original research articles, systematic reviews, and meta-analyses in English. Results: PDT effectively reduces the expression of critical biomarkers such as p53, Cyclin D1, and Ki-67 in AK and other cancerous lesions, leading to reduced cell proliferation and increased apoptosis. Additionally, PDT promotes extracellular matrix remodeling and stimulates collagen production, which has a rejuvenating effect on the skin and a promising role in the treatment of chronic wounds. Conclusions: PDT represents a powerful and versatile treatment option for various dermatological conditions due to its ability to target cellular pathways involved in proliferation and apoptosis. Further research into optimizing treatment parameters and combining PDT with other targeted therapies may enhance patient outcomes, reduce resistance, and pave the way for more individualized therapeutic approaches in dermatology.
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