Sunday, June 24, 2018 by: Russel Davis
Tags: age-related diseases, autophagy, cell, cell function, cellular health, disease treatment, life science, nutrition
The researchers have discovered that a family of proteins called WIPI proteins facilitate autophagy by serving as scaffolds that connect the signal-directed initiation of the process with the subsequent metabolism of cellular material. The experts report in the journal Nature Communications that one form of WIPI protein called WIPI4 protein signals the cells to regulate the extent of the breakdown process when energy begins to deplete. The process is started by the WIPI1 and WIPI2 proteins, and is subsequently continued by the WIPI3 and WIPI4 proteins.
The scientists have also inferred that the WIPI3 protein serves as an additional lysosome regulator, which then prevents the anabolic pathways of the cell when autophagy occurs. According to the experts, the four WIPI proteins act as platforms for multiple protein to protein and protein to lipid interactions. The research team notes that their results may help the scientific community better understand faulty autophagy mechanisms that lead to age-related diseases. Likewise, the experts stress that the findings may have potential implications in developing new treatment plans for various diseases.
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Autophagy declines over time, animal study finds
An animal study published in the eLife journal has revealed that autophagy may show a significant decline as the body ages. A team of researchers at the Sanford Burnham Prebys Medical Discovery Institute in California examined tiny roundworms called C. elegans to carry out the study. The scientists counted the numbers of autophagosomes (AP) and autolysosomes (ALS) in different body tissues of the animal including intestine, muscle, pharynx and neurons. The APs were also measured at different time points of the animal’s life cycle. The experts used chemical blockers in order to better understand the process.
“We found that there is indeed an age-dependent decline in autophagy over time in all tissues examined. We further provide evidence that the increase in APs results from an impairment at a step after APs are made. So basically the autophagy recycling process becomes incomplete with age by stopping somewhere after APs are formed.This research is important because it helps provide time- and site-of-action information for potential future interventions directed at sustaining autophagy to extend lifespan. Our next step will be to perform biochemical research to further pinpoint exactly how autophagy fails to complete its cycle, possibly providing targets to develop specific interventions,” researcher Malene Hansen tells Science Daily online.
“Exposing how autophagy becomes faulty with age may reveal opportunities for us to therapeutically intervene and correct the process to promote health aging…Our goal is to find links between autophagy and age-related diseases. By identifying distinct points in the process that fail, we hope to find ways to correct the defects and find ways to help people live longer, healthier lives,” Hansen concludes.
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