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Cellular Senescence: Difference between revisions
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* '''Oncogene Activation''': Oncogenes are genes that, when activated or overexpressed, can drive cells into uncontrolled growth and potentially lead to tumor formation. In certain scenarios, the activation or aberrant expression of these genes can be recognized by the cell as a precancerous signal. To counteract the risk of malignancy, the cell initiates a senescent program, effectively halting its own proliferation and thus reducing the risk of tumor development. | * '''Oncogene Activation''': Oncogenes are genes that, when activated or overexpressed, can drive cells into uncontrolled growth and potentially lead to tumor formation. In certain scenarios, the activation or aberrant expression of these genes can be recognized by the cell as a precancerous signal. To counteract the risk of malignancy, the cell initiates a senescent program, effectively halting its own proliferation and thus reducing the risk of tumor development. | ||
* Additionally, other lesser-known factors like epigenetic changes, mitochondrial dysfunction, and chronic inflammation have also been implicated in driving cells toward senescence. As research advances, our understanding of these causative factors and their interplay will pave the way for more effective therapeutic interventions targeting cellular senescence. | * Additionally, other lesser-known factors like epigenetic changes, mitochondrial dysfunction, and chronic inflammation have also been implicated in driving cells toward senescence. As research advances, our understanding of these causative factors and their interplay will pave the way for more effective therapeutic interventions targeting cellular senescence. | ||
== Types and Classifications of Senescent Cells == | |||
In humans, cellular senescence is a complex process and can be induced by various stimuli or stresses. While the term "senescent cells" often refers to cells that have undergone the senescence program in response to these stresses, it's worth noting that there isn't just one type of senescent cell. Instead, there are multiple subtypes or classifications based on the cause of senescence. Here are some of the main types of senescent cells based on the inducers of senescence: | |||
# '''Replicative Senescent Cells''': These cells have become senescent due to repeated cycles of replication and the consequent telomere shortening. When telomeres reach a critically short length, the cell undergoes replicative senescence. | |||
# '''Oncogene-Induced Senescent (OIS) Cells''': These cells enter senescence due to the activation or overexpression of oncogenes, which are genes with the potential to cause cancer. This senescence acts as a protective mechanism, preventing potential tumorigenesis. | |||
# '''DNA Damage-Induced Senescent Cells''': Exposure to agents or factors that cause DNA damage, such as radiation, certain chemicals, or oxidative stress, can induce cells to enter a senescent state as a response to protect against potential malignancies or functional aberrations. | |||
# '''Stress-Induced Premature Senescence (SIPS)''': Various forms of cellular stress, other than DNA damage or oncogene activation, can lead to premature senescence. This includes factors like oxidative stress, mitochondrial dysfunction, or even certain drugs and therapeutic treatments. | |||
# '''Wound Healing-Associated Senescent Cells''': These cells arise as a part of the wound healing process. They can help in tissue repair but might need to be cleared afterward to restore tissue functionality fully. | |||
# '''Developmentally Programmed Senescent Cells''': These are cells that become senescent during embryonic development and play a role in shaping tissues and organs. After fulfilling their function, they are typically cleared from the body. | |||
The senescent state is typically characterized by a halt in cell division, resistance to apoptosis (cell death), and often the secretion of a mix of bioactive molecules known as the senescence-associated secretory phenotype (SASP). The SASP can have both beneficial and detrimental effects, depending on the context. | |||
== Implications for Aging and Disease == | == Implications for Aging and Disease == | ||