Senescent cells maintain viability through adhesion-dependent fragmentation that promotes debris deposition.

Senescent cells survive by forming adhesion-dependent fragments called SCAFs that contain damaged organelles and rupture to release pro-inflammatory proteins.

• Why it matters: Understanding how senescent cells maintain viability and contribute to aging, cancer, and neurodegenerative diseases is crucial for developing targeted therapies, but the mechanisms of debris disposal are unclear.
• What they did: The study used live imaging, proteomics, and immunostaining to analyze senescent cells from humans, mice, and tissues, identifying SCAFs as adhesion-dependent fragments containing damaged mitochondria and amyloid-like material.
• The result: Disruption of cell adhesion reduces SCAF formation and causes cell death, while SCAF rupture releases DAMPs and neurodegenerative proteins, promoting migration, invasion, and external deposition of damaged contents.