Scientists discover how cells repair longevity-promoting ‘recycling system’

Mapping pathway behind cell recycling could help combat aging, age-related diseases and neurodegeneration.

Researchers from the University of Pittsburgh have described for the first time a pathway by which cells repair damaged lysosomes, structures that contribute to longevity by recycling cellular trash. The findings, which have been published in?Nature, are an important step towards understanding and treating age-related diseases driven by leaky lysosomes.

My take on this: Often referred to as the cell’s recycling system, lysosomes contain potent digestive enzymes that degrade, break down and clear out molecular waste. These enzymatic contents are walled off and prevented from damaging other parts of the cell with a membrane that acts like chain link security fencing around a hazardous waste facility. Although breaks can occur in this fence, a healthy cell quickly repairs the damage.

This recycling process by the lysosomes helps to keep cells healthy and biologically young, and this is why the decline in cellular repair is thought to play a role in various age-related diseases, including Alzheimer’s, Parkinson’s and cancer. Understanding how lysosomes repair themselves could lead to new therapies for these devastating diseases.

“Lysosome damage is a?hallmark of aging?and many diseases, particularly neurodegenerative disorders such as Alzheimer’s,” said lead author Jay Xiaojun Tan, PhD, assistant professor of cell biology at Pitt’s School of Medicine and member of the Aging Institute, a partnership between Pitt and UPMC. “Our study identifies a series of steps that we believe is a universal mechanism for lysosomal repair, which we named the PITT pathway as a nod to the University of Pittsburgh.”

To learn more about this repair process, Tan teamed up with senior author Toren Finkel, MD, PhD, director of the Aging Institute and distinguished professor of medicine at Pitt’s School of Medicine.

In the initial experiments, Tan damaged lysosomes in lab-grown cells and then measured the proteins that arrived on the scene. He found that an enzyme called PI4K2A accumulated on damaged lysosomes within minutes and generated high levels of a signalling molecule called PtdIns4P.

Read the full article HERE.

Thanks for reading! If you’ve enjoyed this article, it would mean a lot to me if you could subscribe and share it on LinkedIn!