Submission declined on 25 December 2023 by InterstellarGamer12321 (talk). This submission is not adequately supported by reliable sources. Reliable sources are required so that information can be verified. If you need help with referencing, please see Referencing for beginners and Citing sources.
Where to get help
How to improve a draft
You can also browse Wikipedia:Featured articles and Wikipedia:Good articles to find examples of Wikipedia's best writing on topics similar to your proposed article. Improving your odds of a speedy review To improve your odds of a faster review, tag your draft with relevant WikiProject tags using the button below. This will let reviewers know a new draft has been submitted in their area of interest. For instance, if you wrote about a female astronomer, you would want to add the Biography, Astronomy, and Women scientists tags. Editor resources
|
Cellular senescence refers to the irreversible cessation of cell division and the acquisition of a distinct cellular phenotype. While senescence is a normal biological process, it has gained significant attention in the context of aging and age-related diseases. This Wikipedia page aims to explore the intricate relationship between cellular senescence and the aging process, shedding light on the underlying mechanisms and potential implications for human health.
Overview
editDefinition and Characteristics
editCellular senescence is characterized by a set of phenotypic changes, including enlarged and flattened cell morphology, increased senescence-associated beta-galactosidase activity, and altered gene expression patterns. Cells undergoing senescence typically exhibit a growth arrest that prevents further division.
Triggers of Cellular Senescence
editVarious stimuli can induce cellular senescence, such as telomere shortening, DNA damage, oxidative stress, and oncogene activation. The activation of these triggers initiates signaling pathways that converge on the induction of senescence.
Mechanisms
editTelomere Attrition
editOne of the primary triggers of cellular senescence is the shortening of telomeres, the protective caps at the ends of chromosomes. Telomere shortening occurs with each cell division until a critical length is reached, leading to cell cycle arrest.
DNA Damage Response
editAccumulation of DNA damage, caused by factors such as exposure to radiation or environmental toxins, activates the DNA damage response pathway. This, in turn, can induce senescence as a protective mechanism to prevent the propagation of damaged genetic material.
Senescence-Associated Secretory Phenotype (SASP)
editSenescent cells secrete a variety of signaling molecules, growth factors, and inflammatory cytokines collectively known as the SASP. The SASP can influence the microenvironment and neighboring cells, contributing to tissue aging and promoting age-related pathologies.
Role in Aging
editTissue Aging
editThe accumulation of senescent cells in tissues over time is thought to contribute to the aging process. Senescent cells can negatively impact tissue function by promoting inflammation, impairing regeneration, and altering the extracellular matrix.
Senescence and Age-Related Diseases
editCellular senescence has been implicated in various age-related diseases, including cancer, neurodegenerative disorders, and cardiovascular diseases. Understanding the role of senescence in these conditions is crucial for developing targeted therapeutic interventions.
Therapeutic Implications
editResearchers are exploring strategies to target and eliminate senescent cells as a potential approach to mitigate age-related diseases and promote healthy aging. These interventions, known as senolytics, aim to selectively eliminate senescent cells while sparing normal, healthy cells.
Conclusion
editCellular senescence is a multifaceted process with broad implications for understanding the biology of aging and age-related diseases. Ongoing research in this field holds promise for developing novel therapeutic strategies to enhance healthy aging and improve the quality of life for an aging global population.