Murine study demonstrates Foxn1 deficiency alters epidermal thickness, collagen balance, and senescence across lifespan, highlighting its central role in skin aging and homeostasis.
Key Points
To investigate the role of the transcription factor Foxn1 in modulating skin architecture, redox homeostasis, and age-related tissue remodeling across distinct life stages.
Compared wild-type (Foxn1+/+) and heterozygous knockout (Foxn1+/-) mice across three life stages: young (20 days old), middle-aged (1 year old), and old (2 years old).
Evaluated morphological skin changes, keratinocyte differentiation patterns, collagen subtype ratios (collagen I versus collagen III), p21-associated senescence, and oxidative stress responses.
Foxn1+/- mice exhibited a thinner epidermis, thicker dermis, disrupted keratinocyte differentiation, and an enlarged spinous layer relative to wild-type controls.
Wild-type skin accumulated higher levels of collagen I and exhibited age-related increases in p21 expression, whereas Foxn1+/- skin maintained elevated collagen III and suppressed p21 induction.
Foxn1 regulated hypoxia and cellular oxidative stress responses predominantly in young and middle-aged mice, with these regulatory dynamics declining at advanced age.