Interpreting Autophagy–Lysosome Evidence in Hypertrophic Scars and Keloids: A Narrative Review

Yutao Chi,1,* Xinyi Li,1,* Yuan Gao,1,* Jingyun Li,2 Jun Li11Department of Plastic and Cosmetic Surgery, Women’s Hospital of Nanjing Medical University (Nanjing Women and Children’s Healthcare Hospital), Nanjing, 210004, People’s Republic of China; 2Nanjing Women and Children’s Healthcare Institute, Women’s Hospital of Nanjing Medical University (Nanjing Women and Children’s Healthcare Hospital), Nanjing, 210004, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jun Li, Department of Plastic and Cosmetic Surgery, Women’s Hospital of Nanjing Medical University (Nanjing Women and Children’s Healthcare Hospital), 123 Tianfei Street, Mochou Road, Nanjing, 210004, People’s Republic of China, Tel +8613913999994, Email drlijun123@163.com Jingyun Li, Nanjing Women and Children’s Healthcare Institute, Women’s Hospital of Nanjing Medical University (Nanjing Women and Children’s Healthcare Hospital), 123 Tianfei Street, Mochou Road, Nanjing, 210004, People’s Republic of China, Email drlijingyun@163.comAbstract: The therapeutic relevance of autophagy–lysosome findings in hypertrophic scars (HTS) and keloids remains uncertain. We appraised 78 mechanistic claims across 62 reports in a disease-stratified narrative review, distinguishing static markers from dynamic process measurements and causal evidence. Basal autophagic flux across untreated HTS lesion stages remained unresolved. Findings in keloids indicated context-specific differences in turnover, maturation or clearance, and lysosomal distribution, without establishing a uniform lesion-wide state. Treatment studies reported cellular and scar responses but seldom established mediation by autophagy. These findings do not support indiscriminate therapeutic activation or inhibition of autophagy. PubMed-centered coverage, incomplete retrieval records, access constraints and uneven appraisal depth limit interpretation. Failure to establish a mechanism does not show that it is absent from scar biology. Clinical translation requires disease-, stage- and process-matched testing, intervention after lesion establishment for treatment claims, meaningful scar outcomes, assessment of repair safety and follow-up after treatment withdrawal.Keywords: hypertrophic scar, keloid, autophagic flux, lysosome, pathological scarring, lysosomal exocytosis