Senescence, DNA damage and repair in COPD
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Chronic obstructive pulmonary disease (COPD) is an age-associated disease caused mainly by cigarette smoking. Deregulated repair, tissue destruction, inflammation and lung regression are the hallmarks of COPD. Cellular senescence is a signal transduction program leading to irreversible cell cycle arrest. The growth arrest can be triggered by several different mechanisms,including recognition of DNA double-strand breaks by cellular sensors, leading to the activation of cell cycle checkpoint responses and recruitment of DNA repair machinery to damaged foci. The execution of regenerative programs...
Chronic obstructive pulmonary disease (COPD) is an age-associated disease caused mainly by cigarette smoking. Deregulated repair, tissue destruction, inflammation and lung regression are the hallmarks of COPD. Cellular senescence is a signal transduction program leading to irreversible cell cycle arrest. The growth arrest can be triggered by several different mechanisms,including recognition of DNA double-strand breaks by cellular sensors, leading to the activation of cell cycle checkpoint responses and recruitment of DNA repair machinery to damaged foci. The execution of regenerative programs in lung and remote organs is closely linked to viability or senescence of resident cells as well as progenitor cells derived from the circulation. The book is an insight of the work that proposes COPD as a disease of premature lung senescence and DNA damage.
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