BioAcyl Corp
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Manov, I., Odeh, A., & Shams, I. (2020). Aging without inflammaging: Lesson from Spalax. Aging (Albany NY), 12(16), 15875–15877. Added by: Dr. Enrique Feoli (10/06/2025, 01:19) Last edited by: Dr. Enrique Feoli (10/06/2025, 01:23) |
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| Resource type: Journal Article DOI: 10.18632/aging.103953 ID no. (ISBN etc.): 1945-4589 BibTeX citation key: Manov2020 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Inflammaging Creators: Manov, Odeh, Shams Collection: Aging (Albany NY) |
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| Abstract |
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Senescent cells are unable to divide and, thus, they possess a barrier for transmission of mutations for the next generations of cells. However, senescent cells remain alive and reportedly accumulate in tissues with age and, noteworthy, exhibit increased secretion of inflammatory cytokines, chemokines and growth factors (senescent secretome or senescent-associated secretory phenotype, SASP). SASP appears to be beneficial early in life by contributing to embryonic development, wound healing and suppression of malignancy, but deleterious for aging organisms promoting sterile inflammation and leading to age-related disorders, including cancer. This is consistent with the theory of antagonistic pleiotropy of aging, which implies the contribution of pleiotropic genes that have evolved to maintain fitness in youth when selection is strong, but they become harmful when selection weakens with age and reproductive period is over (Reviewed in [1]).
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| Notes |
Schematic diagram showing the differences between canonical inflammatory SASP (human / mouse) and non-inflammatory secretome (NIS) in Spalax and their effects on homeostasis in aging tissues. Canonical secretome of senescent cells comprises a specific pattern of inflammatory mediators and growth factors that may induce senescence in surrounding cells, an effect known as "bystander senescence". The accumulation of senescent cells in aging leads to the amplification of SASP, which in turn modulates the surrounding tissues and causes the so-called "sterile inflammation"- a microenvironment that supports most age-related pathologies, including malignant neoplasms. Due to the efficient DNA repair and other mechanisms, Spalax senescent cells do not produce the main inflammatory factors that are involved in the development of age-related pathologies. Hence, when these cells transmit senescence to surrounding cells via the paracrine factors of "non-inflammatory secretome" (NIS), the recipient cells also do not elicit an inflammatory response and therefore cannot maintain "sterile inflammation" and cancer development in older Spalax. |