Title:Reversing stress damage

Researchers at Georgetown Lombardi Comprehensive Cancer Center recently found that aging cells can be an underlying cause of kidney damage. Working with mice, they studied stress and tissue damage initiated by angiotensin II, a molecule that is known to increase blood pressure and stiffening in the linings of blood vessels.

Results showed cellular senescence, a process by which a cell ages and permanently stops dividing but does not die. Importantly, when the researchers eliminated senescent cells from the mice, tissues returned to a normal state in spite of a continued infusion of angiotensin II.

The researchers chose angiotensin II as the tool to best induce chronic stress because they could regulate its administration and induce a measured stress level similar to that seen in people who see a slow rise in blood pressure over a lifetime.

“There is a pressing need to address the serious systemic effects of high blood pressure and come up with novel treatments to avoid or reverse damage to the kidneys,” says Anton Wellstein, MD, PhD, professor of oncology and pharmacology at Georgetown Lombardi and corresponding author for the article published last December in Frontiers in Cell and Developmental Biology.

Wellstein explains that people can be given angiotensin-lowering drugs to treat their high blood pressure, but they have to be given continuously for a lifetime and may need to be combined with other drugs to improve their efficacy.

“Essentially, we’re building the biological basis for a new therapeutic approach to address the senescence aspect of disease that has mostly been unexplored and untreated,” he says. “Eliminating senescent cells with a tolerable, short-term therapy could potentially alleviate chronic cardiovascular disease and reduce the need for a lifetime of therapy.”

The researchers don’t think anti-senescence drugs are going to be the fountain of youth, but they hope to be able to reverse some premature tissue damage.

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