Scholarlink

<p>Autophagy – the cell’s built-in recycling and quality-control programme – touches every layer of cutaneous biology. In keratinocytes it sculpts the cornified envelope; in melanocytes it balances pigment synthesis and oxidative stress; in immune and appendageal cells it fine-tunes defence, repair and hair-follicle cycling. When this choreography falters, skin disorders emerge. This review journeys from basic mechanisms (ULK1 signalling, Beclin-1/VPS34 nucleation, LC3B lipidation, selective mitophagy) to their fingerprints in health and disease. We dissect how autophagy malfunctions drive psoriasis hyper-proliferation, atopic-dermatitis barrier leakiness, vitiligo depigmentation and the metabolic rewiring of melanoma. Non-melanoma cancers, infectious dermatoses, wound repair, ageing and photo-damage are mapped onto the same autophagic atlas. Therapeutically, the pathway is a double-edged sword. mTOR or caloric-restriction mimetics jump-start a protective flux; chloroquine derivatives and ULK1 blockers clip tumour survival circuits; cannabinoids, photodynamic therapy and immune-checkpoint combinations exploit context-specific toggling between induction and brake. Emerging biomarkers (LC3B-II, p62, AMBRA1) promise patient-stratified interventions. By weaving together molecular detail, pre-clinical insight and clinical translation, we show why autophagy is no longer a backstage process but a star player in dermatology – and how targeting its switches could reshape future treatment algorithms.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Autophagy and mitophagy in dermatological disease: a comprehensive review from molecular pathways to therapeutic frontiers

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月6日

查看全文
  • Luca D’Ambrosio,
  • Maria Elisabetta Greco,
  • Maurizio Forte,
  • Daniele Vecchio,
  • Sonia Schiavon,
  • Flavio Di Nonno,
  • Shazia Tahir,
  • Vittorio Picchio,
  • Claudia Cozzolino,
  • Gianmarco Sarto,
  • Marco Bernardi,
  • Luigi Spadafora,
  • Beatrice Simeone,
  • Mattia Vinciguerra,
  • Sebastiano Sciarretta,
  • Giacomo Frati,
  • Ernesto Greco,
  • Concetta Potenza,
  • Ilaria Proietti,
  • Jacopo Morroni,
  • Elisa Dietrich,
  • Leonardo Schirone

摘要

Autophagy – the cell’s built-in recycling and quality-control programme – touches every layer of cutaneous biology. In keratinocytes it sculpts the cornified envelope; in melanocytes it balances pigment synthesis and oxidative stress; in immune and appendageal cells it fine-tunes defence, repair and hair-follicle cycling. When this choreography falters, skin disorders emerge. This review journeys from basic mechanisms (ULK1 signalling, Beclin-1/VPS34 nucleation, LC3B lipidation, selective mitophagy) to their fingerprints in health and disease. We dissect how autophagy malfunctions drive psoriasis hyper-proliferation, atopic-dermatitis barrier leakiness, vitiligo depigmentation and the metabolic rewiring of melanoma. Non-melanoma cancers, infectious dermatoses, wound repair, ageing and photo-damage are mapped onto the same autophagic atlas. Therapeutically, the pathway is a double-edged sword. mTOR or caloric-restriction mimetics jump-start a protective flux; chloroquine derivatives and ULK1 blockers clip tumour survival circuits; cannabinoids, photodynamic therapy and immune-checkpoint combinations exploit context-specific toggling between induction and brake. Emerging biomarkers (LC3B-II, p62, AMBRA1) promise patient-stratified interventions. By weaving together molecular detail, pre-clinical insight and clinical translation, we show why autophagy is no longer a backstage process but a star player in dermatology – and how targeting its switches could reshape future treatment algorithms.