Wound infiltrating adipocytes are not myofibroblasts

Area of Science:

• Cell Biology
• Regenerative Medicine
• Tissue Repair

Background:

• The cellular origins of scar tissue and myofibroblasts in wound healing are not fully understood.
• A prevailing hypothesis suggests adipocytes (fat cells) may convert into myofibroblasts, contributing to scar formation.

Purpose of the Study:

• To investigate the plasticity and potential fibrogenic capacity of adipocytes following skin injury.
• To determine if adipocytes contribute to myofibroblast differentiation and scar tissue development.

Main Methods:

• Utilized genetic lineage tracing and live imaging in animal models and explants.
• Performed in vitro and in vivo functional assays, including transplantation into wounds.
• Conducted single-cell and bulk transcriptomics to analyze cellular identity and gene expression.

Main Results:

• Skin injury induces a transient migratory state in adipocytes, distinct from fibroblast behavior.
• Migratory adipocytes do not contribute to scar formation and exhibit non-fibrogenic properties.
• Transcriptomic analysis confirmed that adipocytes do not convert into fibrogenic myofibroblasts post-injury.

Conclusions:

• Injury-induced adipocytes remain lineage-restricted and do not reprogram into a fibrosing phenotype.
• These findings challenge existing models of wound healing and scar formation.
• The results have significant implications for regenerative medicine, wound repair, and treating fibrotic diseases.