Vascular stress contributes to age-associated vision loss

What is it about?

Dr. Gangaraju and colleagues used a novel mouse model that overexpresses TNF in endothelial cells to assess the contribution of pre-mature senescence to age-induced visual deficits. In this model, 5 and 10-month-old mice exhibit relevant human equivalencies of a mature adult (approximately 35-year-old) and middle-aged (approximately 50-year-old) patients. Both age groups exhibited visual deficits, and the loss of visual acuity was age-dependent. Markers of inflammation and endothelial cell activation/senescence also exhibited age-dependent increases. These findings suggest that endothelial cell senescence contributes to loss of vision and provide new insights regarding the pathophysiology of retinal diseases.

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Why is it important?

Vision loss adversely impacts quality of life. As people age, their risk for eye diseases and vision loss increases. During aging, some cells stop growing and functioning. These “senescent” cells can also have bystander effects on other cells and prevent them from performing their functions. Activation of the endothelial cells lining the small vessels in the eye results in a severe inflammatory response that includes a release of 10-month-old cytokine TNFα. TNFα is elevated in several retinal diseases, and Dr. Gangaraju’s group has previously shown that TNFα results in premature senescence in endothelial cells. Nonetheless, the role of endothelial cells in age-associated senescence and its bystander effects on other retinal cells are not known.

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