Table 1.

Targeting mTOR to delay cellular senescence

Model	Description	Senescence inducing methods	Effect of rapamycin	Ref.
HT1080-p21	Human fibrasarcoma	IPTG-induced p21 expression	Reduce SA-β-gal activity	[30]
HT1080-p21	Human fibrasarcoma	IPTG-induced p21 expression	Re-enter cell cycle when inducing agents are removed. Remain large size	[50]
HT1080-p16	Human fibrasarcoma	IPTG-induced p16 expression	Preserve the proliferative capacity	[50]
ERas	Rodent fibroblast	Sodium butyrate-induced p21	Marginal decrease in SA-β-gal, no change in morphology, yet prevent the loss of proliferative potential	[50]
WI-38	Human primary lung fibroblast	DNA damage by Doxorubicin	Partially prevented senescent phenotype	[30]
ARPE-19	human retinal pigment epithelial cell	H2O2	Reduce SA-β-gal activity, did not change flat morphology, prevent the permanent loss of proliferation	[50]
BJ	Human skin fibroblasts	Continuous passage	Suppress IL-8 and p21 but not SA-β-gal activity and flattened morphology in senescent cells	[52]
BJ	Human skin fibroblasts	Continuous passage	Treatment of pre-senescent cells delay SA-β-gal, no change in cell morphology	[52]
BJ	Human skin fibroblasts	RAS overexpression	Higher proliferation rate and less SA-β-gal	[52]
MEFs	Mouse embryonic cells	Continuous passage	Partially suppress senescent marker. Cells adapt to rapmycin, not useful for long term treatment.	[53]
REFs	Rat embryonic cells	Continuous passage	Reverse SA-β-gal and DNA damage marker H2AX and 53BP1	[53]
Wnt1 transgenic mice	Doxycycline-inducible K5rtTA/tet-Wnt1 mice	Persistent activation of Wnt1	Partially suppressed disappearance of the epidermal stem cell compartment and subsequent hair loss	[54]