The Fountain of Youth

A step toward discovering the fountain of youth could involve protecting against the inevitable accumulation of “senescentcells associated with aging and age-related diseases. Now, researchers from Japan have identified the MondoA protein as key to protecting against the accumulation of senescent cells.

In a study published this month in Cell Reports, researchers led by Osaka University have shown that MondoA delays cellular senescence, and therefore promotes longevity, by activating . Autophagy is a process whereby cells undergo controlled breakdown and recycling of their components, which is important for maintaining stable conditions in the cellular environment and for enabling adaptation to stress. Activation of autophagy by MondoA partly involves suppressing a protein called Rubicon, which is a negative regulator of autophagy. Rubicon can increase with aging in various tissues and model organisms, which can cause the decline in autophagy seen with aging.

Furthermore, MondoA is also essential to maintaining stable conditions of parts of the cell called mitochondria, which are responsible for energy production. MondoA does this by regulating another molecule, Prdx3, which is involved in mitochondrial turnover. Mitochondria are constantly fusing and dividing, which is important for maintaining their health. Prdx3 is part of the process by which autophagy occurs in mitochondria, preventing senescence. The research team led by Osaka University concluded that MondoA plays a key role in the regulation of Prdx3 and therefore in maintaining mitochondrial stability.

Particularly dense accumulation of senescent cells has been observed in the kidney. The researchers therefore looked at ischemic acute kidney injury (AKI) in mice.

Mice with ischemic AKI and reduced levels of MondoA showed increased senescence,” explains lead author Hitomi Yamamoto-Imoto. “We also found that decreased MondoA in the nucleus correlated with human aging and ischemic AKI. MondoA therefore counteracts cellular  in aging and ischemic AKI in both mice and humans.”

Drugs that eliminate senescent cells, called senolytics, are currently being considered as treatment for age-associated diseases. However, senescent  play important roles, and their complete removal may have considerable side effects. “Our work shows that the transcriptional activation of MondoA can protect against , kidney injury associated with aging, and organismal aging,” explains senior author Tamotsu Yoshimori. “Activation of MondoA and therefore autophagy could be a potentially safe therapeutic strategy.” This work could well open new and safer avenues for the treatment of aging and age-related diseases.

Source: https://phys.org/

How To Heal Acute Kidney Injury

Each year, there are some 13.3 million new cases of acute kidney injury (AKI), a serious affliction. Formerly known as acute renal failure, the ailment produces a rapid buildup of nitrogenous wastes and decreases urine output, usually within hours or days of disease onset.  Severe complications often ensue. Currently, there is no known cure for AKI.

AKI is responsible for 1.7 million deaths annually. Protecting healthy kidneys from harm and treating those already injured remains a significant challenge for modern medicine.

In new research appearing in the journal Nature Biomedical Engineering, Hao Yan and his colleagues at the University of Wisconsin-Madison and in China describe a new method for treating and preventing AKI. Their technique involves the use of tiny, self-assembling forms measuring just billionths of a meter in diameter.

Yan directs the Biodesign Center for Molecular Design and Biomimetics and is Professor in the School of Molecular Sciences at the Arizona State University (ASU).

Their research demonstrated that the introduction of DNA origami nanostructures (DONs) protected normal kidneys and improved functioning of kidneys damaged by AKI. The beneficial effect of the nanostructures was comparable to the current treatment modality, administration of an anti-oxidant drug known as N-acetylcysteine (NAC). New treatments are being saught because NAC is not easily absorbed in the kidneys. Further examination of stained tissue samples from mice confirmed the beneficial effects of the DONs.

Source: https://biodesign.asu.edu/