Smoke Particles Cause Blood Vessel Aging and Inflammation That Are Reduced by Blocking Both mTORC1 and mTORC2 with Rapalink-1

Rapalink-1 treatment reduced oxidative stress and DNA damage in vascular cells exposed to smoke condensate.

• Smoke condensate exposure increased reactive oxygen species and DNA damage in vascular cells.
• Senescence-associated changes included heightened senescence markers such as elevated β-galactosidase activity and increased p21 expression.
• Exposure to smoke condensate led to increased expression of inflammatory and matrix-remodeling genes linked to cellular senescence.
• Rapalink-1 co-treatment attenuated these senescence markers and partially normalized gene expression related to inflammation and extracellular matrix remodeling.
• Mechanistically, smoke condensate activated specific signaling pathways, which were dampened by Rapalink-1.

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