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This study created transgenic mouse models with the LMNA gene mutation common in Hutchinson-Gilford progeria syndrome, revealing skin and teeth abnormalities related to transgene expression levels.

This study reported that inhibiting the JAK-STAT pathway with baricitinib restored cellular homeostasis, delayed senescence, and reduced proinflammatory markers in Hutchinson-Gilford progeria syndrome cell models.

This study found that although progerin expression in mouse skin causes significant nuclear shape changes in keratinocytes, it does not result in alopecia or common skin abnormalities seen in human Hutchinson–Gilford progeria syndrome.

This review discusses the molecular mechanisms of Hutchinson-Gilford progeria syndrome and evaluates current research trends, available mouse models, and prospects for developing therapies, but reports no new clinical findings.

This review explores how cell and mouse models have contributed to understanding the mechanisms of human aging, particularly focusing on Hutchinson-Gilford Progeria Syndrome, and reports no new clinical results.