Alterations of the Cell Nucleus as a Driver of Chronic Inflammation in Aging

Dear Colleagues,

Changes to the nucleus homeostasis can occur due to exposure to oxidative stress; agents causing chromatin disruptions; and DNA damage resulting from losing repair factors or mutations to genes encoding nuclear proteins including nuclear envelope proteins, lamina components, chromatin remodeling, protein kinase, phosphatase, or other modifiers. These various modifications occurring in the nucleus can ultimately drive cells to enter permanent cell cycle arrest and senescence. Senescent cells, beside exhibiting nuclear, cytoplasmic, and morphological changes, are also known to produce a large repertoire of senescence-associated secretary factors that include proinflammatory factors. These secreted inflammatory molecules can propagate to neighboring cells and cause them to enter senescence and secrete similar sets of proinflammatory molecules. This contagious senescence cycle can eventually affect the entire tissue or organ where the senescent cells reside and consequently cause tissue aging, organ dysfunction, and the development of the tissue- or organ-related pathology.

How signals emanate from definite changes to the nucleus and initiate molecular processes that drive cells to senescence remain largely unknown. This Special issue of Cells seeks to expand our understanding of the molecular and cellular mechanisms that are at play in the setting of this vicious cycle of chronic inflammation and starts from the nucleus.

Prof. Dr. Karima Djabali
Guest Editor

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• Nucleus
• Nuclear envelope
• Lamin
• Senescence
• Inflammation
• Aging