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        <identifier>oai:figshare.com:article/33924976</identifier>
        <datestamp>2026-09-18T08:30:23Z</datestamp>
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          <dc:title>Table 1_Platelet-rich therapies in cutaneous and mucocutaneous disorders characterized by inflammatory tissue responses: mechanistic insights and clinical evidence.docx</dc:title>
          <dc:creator>Eduardo Anitua (460933)</dc:creator>
          <dc:creator>Roberto Tierno (25071154)</dc:creator>
          <dc:creator>Mohammad Hamdan Alkhraisat (25071157)</dc:creator>
          <dc:subject>Foetal Development and Medicine</dc:subject>
          <dc:subject>epithelial barrier dysfunction</dc:subject>
          <dc:subject>immunomodulation</dc:subject>
          <dc:subject>inflammation</dc:subject>
          <dc:subject>mucocutaneous diseases</dc:subject>
          <dc:subject>platelet-rich derivatives</dc:subject>
          <dc:subject>tissue regeneration</dc:subject>
          <dc:description>&lt;p&gt;Cutaneous and mucocutaneous dermatoses comprise a heterogeneous group of inflammatory, autoimmune, infectious, and immune-mediated diseases affecting epithelial barrier tissues, including skin and mucosal surfaces. Despite their diverse etiologies these conditions frequently share convergent pathogenic mechanisms characterized by epithelial barrier dysfunction and inflammation, contributing to a substantial global health burden. At the immunopathological level, these disorders frequently involve coordinated activation of innate immune sensing pathways followed by adaptive immune polarization driven by Th1, Th2, Th17 and CD8+ T cell–associated responses. These pathways converge on shared intracellular signaling cascades, resulting in persistent cytokine production, chronic inflammation, and epithelial barrier disruption. Platelet-rich derivatives are autologous biologic therapies enriched in bioactive mediators with pleiotropic regenerative and immunomodulatory properties. Preclinical evidence indicates that these formulations modulate innate immune activation, promote macrophage polarization toward pro-regenerative phenotypes, influence dendritic cell maturation, and support regulatory T cell responses largely via modulation of NF-κB, TLR, PI3K/Akt, MAPK, and TGF-β/SMAD-dependent pathways. In addition to immunomodulation, platelet-rich derivatives enhance tissue repair by promoting cell activation, angiogenesis, and extracellular matrix remodeling. They also contribute to epidermal barrier restoration and normalization of epithelial–immune–microbiome interactions. Despite the heterogeneity of underlying pathogenic molecular pathways, the multi-level effects of platelet-rich formulations provide a rationale for targeting shared downstream processes involved in tissue injury and disease progression. Clinical evidence, although heterogeneous and largely limited to small studies, suggests potential benefit in psoriasis, atopic dermatitis, lichen planus, lichen sclerosus, vitiligo, alopecia areata, and acne, with limited evidence in other mucocutaneous dermatoses associated with substantial primary or secondary inflammation. However, variability in pathophysiological landscapes, platelet-rich formulations and experimental designs limits definitive conclusions. Overall, platelet-derived therapies represent a promising adjunctive approach for restoring immune and epithelial homeostasis in inflammatory mucocutaneous disease, underscoring the need for methodologically standardized clinical and translational research and compliance with minimum reporting standards.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-18T08:30:23Z</dc:date>
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          <dc:identifier>10.3389/fmed.2026.1901254.s001</dc:identifier>
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