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Updated: Jul 12, 2026
08:20
In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
Published on: May 1, 2020
Galectin-1 regulates scar hyperplasia by modulating NASP variable splicing to generate ROS.
1Department of Plastic Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Summary
Galectin-1 is overexpressed in hypertrophic scars and drives their formation by regulating cell activity and promoting PANoptosis. Silencing Galectin-1 reduces scar progression, offering a new therapeutic target for treating hypertrophic scars.
Area of Science:
- Biochemistry
- Cell Biology
- Dermatology
Background:
- Hypertrophic scar (HS) pathogenesis is driven by dysregulated fibrogenic cellular activity.
- The precise role of Galectin-1 in modulating HS development is not fully understood.
Purpose of the Study:
- To investigate the role and molecular mechanisms of Galectin-1 in hypertrophic scar formation.
- To explore Galectin-1 as a potential therapeutic target for HS.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blot to assess Galectin-1 expression.
- Lentivirus-mediated knockdown of Galectin-1 in hypertrophic scar fibroblasts (HSFs).
- RNA sequencing (RNA-seq), immunofluorescence, and RT-PCR to elucidate molecular pathways and alternative splicing.
Main Results:
- Galectin-1 is significantly overexpressed in HS tissues and activated fibroblasts.
- Galectin-1 knockdown reduced HSF proliferation, migration, and invasion, and downregulated fibrotic markers.
- Galectin-1 orchestrates PANoptosis and ferroptosis via the ROS pathway, modulating NASP alternative splicing dependent on HNRNPL.
Conclusions:
- Galectin-1 is a critical regulator of hypertrophic scar formation by influencing fibrotic cascades through PANoptosis.
- Targeting Galectin-1 presents a novel therapeutic strategy for managing hypertrophic scars.
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