Inhibition of JAK-STAT Signaling with Baricitinib Reduces Inflammation and Improves Cellular Homeostasis in Progeria Cells

The study demonstrated that inhibiting the JAK-STAT signaling pathway with Baricitinib reduced inflammation and improved cellular homeostasis in Hutchinson-Gilford Progeria Syndrome (HGPS) cells. Baricitinib treatment decreased progerin levels, improved nuclear morphology, and reduced the expression of proinflammatory factors such as IL6, IL8, IL18, and CCL2. Additionally, it delayed senescence and enhanced mitochondrial function in both normal and HGPS cells. These findings suggested that Baricitinib could be a valuable therapeutic strategy for managing HGPS and other age-related conditions involving chronic inflammation and cellular dysfunction.