Research reveals how aging cells can be an underlying cause of kidney
damage

Date:
December 8, 2021
Source:
Georgetown University Medical Center
Summary:
A study in mice has found that 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, leads to
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.



FULL STORY ==========================================================================
A study in mice by researchers at Georgetown Lombardi Comprehensive
Cancer Center has found that 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, leads to 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 findings appear in Frontiers in Cell and Developmental Biologyon
December 8, 2021.

"We've known that angiotensin II can lead to hypertension and cellular
damage, but our findings show that chronic, stress-induced damage due to slightly elevated blood pressure could be reduced by eliminating senescent cells," says Irfan Khan, an MD/PhD candidate in the Tumor Biology program
at Georgetown University and first author. "By preventing the harmful
effects of angiotensin II, we revealed a novel mechanism for eliminating senescent cells that could potentially be used to develop targeted drugs
to eliminate these cells." 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. This stress typically results in less flexibility in the lining of blood vessels,
which in turn leads to higher blood pressure. The researchers discovered
that these effects are particularly pronounced in the kidneys and not
in the brain or lungs, which is what they expected when they started
their experiments.

"We can give people 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. 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
this article. "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.

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. "A senescence
drug would probably be a very short-term treatment, maybe just a few
days to two weeks," Wellstein says. "Rather than constantly trying to
dampen down high blood pressure, we propose getting rid of the senescent
cells so that a physician could more easily treat the primary causes." ========================================================================== Story Source: Materials provided by
Georgetown_University_Medical_Center. Note: Content may be edited for
style and length.


========================================================================== Journal Reference:
1. Irfan Khan, Marcel O. Schmidt, Bhaskar Kallakury, Sidharth Jain,
Shaunt
Mehdikhani, Moshe Levi, Margarida Mendonca, William Welch, Anna T.

Riegel, Christopher S. Wilcox, Anton Wellstein. Low Dose Chronic
Angiotensin II Induces Selective Senescence of Kidney Endothelial
Cells.

Frontiers in Cell and Developmental Biology, 2021; 9 DOI: 10.3389/
fcell.2021.782841 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2021/12/211208123429.htm

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