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Cellular Senescence: Difference between revisions
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# '''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. | # '''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. | # '''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. | # '''DNA Damage-Induced Senescent Cells''': Exposure to agents or factors that cause DNA damage, such as radiation, certain chemicals, or [[Oxidative Stress|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. | # '''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|oxidative stress]], [[Mitochondrial Dysfunction|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. | # '''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. | # '''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. | ||
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During early to mid-life, several factors contribute to the exponential accumulation of senescent cells: | During early to mid-life, several factors contribute to the exponential accumulation of senescent cells: | ||
# '''Natural Aging Process''': As individuals advance in age, cellular stresses, such as DNA damage, telomere shortening, and oxidative stress, become more prevalent, pushing more cells into the senescent state. | # '''Natural Aging Process''': As individuals advance in age, cellular stresses, such as DNA damage, [[Telomere Attrition|telomere shortening]], and [[Oxidative Stress|oxidative stress]], become more prevalent, pushing more cells into the senescent state. | ||
# '''Compounding Effects''': As more cells become senescent, the senescence-associated secretory phenotype (SASP) can induce senescence in neighboring cells, creating a compounding effect where the rate of new cells entering senescence increases over time. | # '''Compounding Effects''': As more cells become senescent, the senescence-associated secretory phenotype (SASP) can induce senescence in neighboring cells, creating a compounding effect where the rate of new cells entering senescence increases over time. | ||
# '''Environmental and Lifestyle Factors''': Repeated exposure to stressors like ultraviolet radiation, toxins, or an unhealthy lifestyle can further accelerate the accumulation of senescent cells during these years. | # '''Environmental and Lifestyle Factors''': Repeated exposure to stressors like ultraviolet radiation, toxins, or an unhealthy lifestyle can further accelerate the accumulation of senescent cells during these years. | ||
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However, it's not well-established that the growth rate of senescent cells declines substantially in advanced age. The reasons for a potential stabilization or slowdown include: | However, it's not well-established that the growth rate of senescent cells declines substantially in advanced age. The reasons for a potential stabilization or slowdown include: | ||
# '''Depleted Stem Cell Pools''': With age, the body's pool of stem cells, responsible for tissue regeneration and repair, diminishes. Since there are fewer actively dividing cells in very elderly individuals, there may be fewer cells to enter a senescent state. | # '''[[Stem Cell Exhaustion|Depleted Stem Cell Pools]]''': With age, the body's pool of stem cells, responsible for tissue regeneration and repair, diminishes. Since there are fewer actively dividing cells in very elderly individuals, there may be fewer cells to enter a senescent state. | ||
# '''Natural Cellular Attrition''': Over time, some senescent cells might undergo natural cell death, even if they are initially resistant to apoptosis. | # '''Natural Cellular Attrition''': Over time, some senescent cells might undergo natural cell death, even if they are initially resistant to apoptosis. | ||
# '''Tissue Atrophy and Reduced Cellularity''': Some tissues lose cell density with advanced age, potentially contributing to the reduced absolute numbers of senescent cells. | # '''Tissue Atrophy and Reduced Cellularity''': Some tissues lose cell density with advanced age, potentially contributing to the reduced absolute numbers of senescent cells. | ||