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DNA Damage can Stall the Cell Cycle02:37

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Updated: Aug 11, 2025

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
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Inflammation and DNA damage: cause, effect or both.

Antonio Pezone1, Fabiola Olivieri2,3, Maria Vittoria Napoli2

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Chronic inflammation triggers DNA damage and cell senescence, creating a cycle that can lead to organ dysfunction in various diseases. This process involves the DNA damage response (DDR) and senescence-associated secretory phenotype.

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Area of Science:

  • Cellular biology
  • Immunology
  • Genetics

Background:

  • Inflammation is a biological response to stimuli, but unresolved inflammation involves chronic cytokine secretion and redox stress.
  • Redox imbalance can cause DNA damage, activating the DNA damage response (DDR) orchestrated by ATM and ATR kinases.
  • DDR-mediated senescence, involving p53, p16, and p21, arrests the cell cycle and promotes a senescence-associated secretory phenotype.

Purpose of the Study:

  • To explore the intricate relationship between inflammation, DNA damage, and DDR-mediated senescence.
  • To elucidate the role of this interconnected circuitry in various diseases.

Main Methods:

  • Literature review and synthesis of existing research on inflammation, DNA damage, and senescence.
  • Analysis of the molecular mechanisms involving ATM, ATR, p53, p16, and p21.
  • Examination of the senescence-associated secretory phenotype and its implications.

Main Results:

  • A vicious cycle exists where inflammation, DNA damage, and DDR-mediated senescence perpetuate each other.
  • This conserved circuitry arrests the cell cycle to prevent mutations during redox stress.
  • Organ dysfunction in autoimmune, rheumatic, degenerative, and vascular diseases may stem from inflammation driven by DNA damage-induced senescence.

Conclusions:

  • The interplay between inflammation, DNA damage, and senescence is a fundamental biological process.
  • This process contributes to the pathogenesis of diverse diseases characterized by organ dysfunction.
  • Targeting this cycle holds potential for therapeutic interventions in multiple conditions.