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How do SASPs contribute to cancer, diabetes and aging?
In biomedical research, the aging-associated secretory phenotype (SASP) has received widespread attention. This is a phenotype associated with aging cells that secrete large amounts of inflammatory cytokines, immunomodulatory factors, growth factors, and proteases. With the deepening of research, the composition of SASP is increasingly considered to be the culprit in causing a variety of aging-related diseases.
Research shows that SASP may include exosomes and extracellular bodies, which contain enzymes, microRNA, DNA fragments and other biologically active factors.
SASP initially behaves as immunosuppressive, and then changes to a state of intense inflammatory response. This transformation process causes lasting damage to cells during the aging process. These secretions not only affect the function of surrounding healthy cells, but the cumulative impact may lead to an increased risk of various chronic diseases such as cancer and diabetes.
The production of SASP is regulated by many transcription factors, especially the NF-κB, IL-1α and mTOR pathways. These factors interact to promote the inflammatory response of aging cells, creating a persistent, tissue-damaging chemical environment.
Although SASP can attract immune cells to eliminate aging cells, continued SASP can promote the development of cancer.
This phenomenon is particularly obvious among the elderly. Chronic inflammation not only reduces the body's resistance to foreign pathogens, but also increases the incidence of various aging-related diseases. In fact, research points out that as older adults’ immune systems weaken, so do their ability to resist infectious diseases like COVID-19.
At a metabolic level, SASP may also lead to insulin resistance and other endocrine disorders, which further exacerbate the development of aging-related diseases. This is because SASP factors such as IL-6 and TNFα will induce the aging of surrounding cells in batches, forming a vicious cycle, not only in the affected cells, but also further interfering with the function of healthy cells.
Therefore, SASP is like a double-edged sword. Although short-term SASP helps cell repair and regeneration, the long-term effects may be severe damage.
Rethinking this impact has led researchers to seek new treatments, including senolytics, a treatment strategy that targets the elimination of senescent cells and is intended to mitigate the long-term effects of SASP. Studies have shown that certain natural compounds (such as flavonoids) have a significant effect on inhibiting the production of SASP.
The key to healthy aging lies in balancing the beneficial and harmful effects of SASP. Perhaps in the future medical field, personalized treatment based on SASP components will become the norm to achieve the best therapeutic effect.
In summary, although SASP has multiple functions in the cellular aging process, its impact on chronic diseases cannot be underestimated. In the future, how should we manage SASP more effectively to reduce the risk of aging-related diseases?
