Cellular Senescence

Senescent cells are cells that no longer divide. These cells acquire a large and flat cellular appearance, decrease contacts with other cells, and increase adhesion to the extracellular matrix. In normal replicative senescence, the cell simply enters senescence after a certain number of replications. However, stress-induced senescence causes cells to initiate senescence prematurely due to a variety of stresses. In fact, some hypothesize that the senescence program originally evolved as an antiviral mechanism. This burgeoning field may also yield other important clues about the cellular biology of aging. Molecularly, the cellular senescence program activates p53 and pRb signaling, leading to withdrawal from the cell cycle. Stress pathways that may cause cellular senescence include DNA damage, oxidative stress, interferon-related responses, and signaling via either insulin growth factors (IGF) or mitogen activated protein kinases (MAPK). Due to cellular senescence activation in early stage cancers and its dysregulation in late stage cancers, understanding and controlling the process holds significant therapeutic promise. ...

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Senescent cells are cells that no longer divide. These cells acquire a large and flat cellular appearance, decrease contacts with other cells, and increase adhesion to the extracellular matrix. In normal replicative senescence, the cell simply enters senescence after a certain number of replications. However, stress-induced senescence causes cells to initiate senescence prematurely due to a variety of stresses. In fact, some hypothesize that the senescence program originally evolved as an antiviral mechanism. This burgeoning field may also yield other important clues about the cellular biology of aging. Molecularly, the cellular senescence program activates p53 and pRb signaling, leading to withdrawal from the cell cycle. Stress pathways that may cause cellular senescence include DNA damage, oxidative stress, interferon-related responses, and signaling via either insulin growth factors (IGF) or mitogen activated protein kinases (MAPK). Due to cellular senescence activation in early stage cancers and its dysregulation in late stage cancers, understanding and controlling the process holds significant therapeutic promise.