Cellular senescence

Biological process · 3 studies in the Atlas

State in which a cell permanently stops dividing but stays alive, secreting inflammatory signals (the SASP). Senescent cells accumulate with age and drive age-related disease. mTOR both promotes the senescent state and powers its inflammatory secretions.

Evidence at a glance

TierWhat it meansStudies
BDirect human evidence1
DMechanistic / in vitro / review2

Studies

StudyYearTierFinding
CHU20192019BA small human trial testing whether rapamycin can slow aging in a tissue you can actually see and biopsy - skin. Topical rapamycin significantly lowered the senescence marker p16 and raised collagen V
LAB20152015DExplained HOW rapamycin calms 'inflammaging'. Senescent cells spew inflammatory signals (the SASP) that damage surrounding tissue and even feed tumors. mTOR powers this by translating IL1A, the cytoki
DEM20092009DBlagosklonny's key experiment behind his 'hyperfunction' theory of aging. When a cell's division is blocked but mTOR keeps driving growth, the cell tips into permanent senescence. Rapamycin uncouples

Related entities

mTORC1 3Rapamycin 3mTOR 14E-BP1 1Skin aging 1

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