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Updated: Oct 28, 2026

A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
Published on: November 29, 2024
Interpreting Autophagy-Lysosome Evidence in Hypertrophic Scars and Keloids: A Narrative Review
Yutao Chi1, Xinyi Li1, Yuan Gao1
1Department 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.
Abstract:
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.
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