Lamin A mutation mouse models​ are genetically engineered strains that carry mutations in the LMNAgene, which encodes the Lamin A/C proteins. These proteins are key structural components of the nuclear lamina—a fibrous meshwork lining the inner nuclear membrane that provides mechanical support to the nucleus and regulates crucial cellular processes like gene expression, DNA replication, and cell signaling. Mutations in the human LMNAgene cause a spectrum of disorders known as laminopathies. These include muscular dystrophies, cardiomyopathies, lipodystrophies, and premature aging syndromes like Hutchinson-Gilford Progeria Syndrome (HGPS). Mouse models with targeted LMNA mutations are essential tools for understanding the pathophysiology of these diverse diseases and for developing therapeutic strategies. Lmna^(G609G/G609G) mice：These models carry a silent point mutation that activates a cryptic splice site, leading to the production of a toxic, permanently farnesylated protein called progerin.Mice expressing progerin display dramatic premature aging phenotypes, including growth retardation, loss of subcutaneous fat, osteoporosis, cardiovascular abnormalities, and significantly shortened lifespan. They are the primary tool for studying HGPS and the role of lamins in normal aging.