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How a broken DNA repair tool accelerates aging

January 30, 2026 How a broken DNA repair tool accelerates aging by Goethe University Frankfurt am Main edited by Gaby Clark, reviewed by Robert Egan Editors' notes This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: fact-checked peer-reviewed publication trusted source proofread The GIST Add as preferred source The failure of the repair enzyme SPRTN in these cultured cells leads to fatal errors in cell division, e.g. by distributing the chromosomes (red) to three daughter cell nuclei instead of two (arrow). Green: Cell division apparatuscytoskeleton. Credit: Institute of Biochemistry II, Goethe University Frankfurt Although DNA is tightly packed and protected within the cell nucleus, it is constantly threatened by damage from normal metabolic processes or external stressors such as radiation or chemical substances. To counteract this, cells rely on an elaborate network of repair mechanisms. When these systems fail, DNA damage can accumulate, impair cellular function, and contribute to cancer, aging, and degenerative diseases. One particularly severe form of DNA damage are the so-called DNAprotein crosslinks (DPCs), in which proteins become attached to DNA. DPCs can arise from alcohol consumption, exposure to substances such as formaldehyde or other aldehydes, or from errors made by enzymes involved in DNA replication and repair. Because DPCs can caus

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