The Emerging Role of Senescence in Ocular Disease

Table 3

Mitochondrial metabolic changes in senescence.

Cell type	Source of senescence	Mitochondrial mass	Oxidative phosphorylation	Glycolysis	Mitochondrial ATP production	References
Human MRC5 fibroblasts	RS	Increased	Increased	Increased	Decreased	[172]
Human foreskin fibroblasts	RS	Increased	Increased	Increased	Increased	[169]
Human dermal fibroblasts.	RS	No change	No change	Increased	No change	[50]
Human dermal fibroblasts.	Doxorubicin	Increased	Increased	No change	Increased	[50]
Human foreskin fibroblasts	Doxorubicin	Increased	Increased	Increased	Increased	[169]
Human diploid IMR90 fibroblasts	Oncogenic Ras-induced senescence (OIS)	Increased	Decreased	-	Decreased	[56
Human Dermal Fibroblasts	Oncogene-induced senescence (OIS)	NA	Increased	-	-	[167]
Human fetal lung fibroblasts	Oncogene-induced senescence (OIS)	-	Increased	-	-	[166]
Human fibroblasts	Radiation induced	-	No change	Increased	-	[173]
Mouse melanoma B16-F1 cell line	Temozolomide (genotoxic agent)	Increased	Increased	Decreased	increased	[174]
HEI-OC1 auditory cells	SIPS (H2O2)		Decreased	-	No change	[175]
Human lung fibroblasts	SIPS (H2O2)	-	Increased	-	Increased	[176]
Human lung and cardiac fibroblast cells	SIPS (nucleoside analogs)	Increased	Increased	-	Increased	[177]
Human disc cells	SIPS	Increased	Increased	-	Increased	[168]
Human fibroblasts	γ radiation	-	No change	Increased	-	[173]

RS: replicative senescence; OIS: oncogene-induced senescence; SIPS: stress-induced premature senescence.