Ageing answers no longer a hard cell


Judith Campisi at the Future of Experimental Medicine Conference.

The holy grail of healthy old age may lie in the riddle of cells that stop cancer and hasten age at the same time.

Professor Judith Campisi, the head of research labs at San Francisco’s Buck Institute for Research on Ageing and the Lawrence Berkeley National Laboratory, presented this research at our Inflammation in Disease and Ageing conference in Manly.

She has found that senescent cells, which stop cancer in its tracks, also promote the inflammation that drives many age-related problems and chronic diseases.

“The good news is that if we can work out a way to maximise the beneficial effects of cell senescence in fighting cancer and wound healing, and minimise the deleterious effects of inflammation in old age, we might reach the Holy Grail of staying healthier for longer,” Professor Campisi says.

“Her work helps us understand the links between inflammation and ageing, which is a key theme of Centenary Institute’s research,” says Professor Jennifer Gamble, one of the conference organisers and the leader of the institute’s Vascular Biology Research Group.

Senescent cells develop as a natural defence to suppress cell growth induced by potentially cancer-inducing stress. The cells stop dividing and can no longer form tumours, but the cells remain alive.

Professor Campisi has found that senescent cells secrete compounds that promote inflammation in the surrounding tissue, a natural part of wound healing.

However, in older people the inflammation can contribute to a range of age-related problems, such as cataracts, chronic diseases and, ironically, late-life cancer.

She has also found that senescent cells accumulate with age in vertebrae tissue and around areas of existing degeneration.

Together with colleagues at the Mayo Clinic, Professor Campisi has shown that eliminating senescent cells in older mice can lead to a healthier, and potentially longer, life.

“Judith Campisi’s research explains why the elderly are at such risk of developing chronic disease,” says Prof Gamble. “It also shows how what happens at the cellular level can have an impact on the whole body. Diabetes, for example, produces a build-up of senescent cells, and that in itself leads to problems with wound healing.

“In my own work, we know that the endothelial cells that form the blood vessels are subject to a lot of stress, induced by such things as changes in blood pressure and diet. My laboratory has already picked up pro-inflammatory senescent cells in endothelial tissue. Interestingly, we have also discovered the first senescent cells which are anti-inflammatory.”

The Manly symposium, organised by the Centenary Institute, is the first of a series of biennial conferences on the Future of Experimental Medicine.

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