Cellular senescence contributes to many age-related diseases. Senescent cells arise naturally as a result of the Hayflick limit on cellular replication, as well as injury, or due to molecular damage or a toxic environment that might give rise to cancer. A senescent cell ceases replication and secretes a potent mix of signals that produce inflammation and disrupt nearby tissue structure and function. In youth, senescent cells are near all quickly removed, via programmed cell death or the actions of the immune system, but these removal mechanisms falter with age. Senescent cells accumulate as a result, and the more of them there are, the worse the outcome. These errant cells are thought to be responsible for a sizable fraction of the chronic inflammation of aging, for example, and produce many other ill effects besides.

While good evidence has existed for decades to point to senescent cells as an important cause of aging, the research community at large has only gradually accepted this hypothesis over the last decade. Thus the contribution of senescence to age-related disease is only well studied in a handful of the hundreds of varied age-related diseases. This is very much the case for the eye. There is some recent evidence for senescence to be involved in cataracts and glaucoma, but for any number of other conditions the role of senescence remains to be investigated in depth.

This situation is repeated throughout the body. Since the first senolytic therapies capable of selectively destroying a meaningful fraction of senescent cells already exist, it seems likely that advances in knowledge will be driven by trying the treatments and watching the results, rather than by more passive investigation. This is probably for the best, and certainly much faster if the goal is rapid progress towards effective treatments that can turn back age-related conditions by addressing deeper causes.

The Emerging Role of Senescence in Ocular Disease