Blocking autophagy to prevent old age organ decline? Find out

Subhangi Das, Bankura Sammilani College

According to a new study published in Nature Cell Biology, to stop the cannibalistic behaviour of an enzyme that can be the key to new drugs that fight against the age-related diseases. Researchers for the first time found out a process showing how the self-eating cellular method which is known as autophagy causes the SIRT1 enzyme, in the Perelman School of Medicine, University of Pennsylvania. This enzyme also plays a role in longevity to degrade over time in cells and tissues in mice. Cells are leaky faucets, which drips away from the level of proteins and enzymes, like SIRT1.

After the body age, it can lead to chronic diseases, organ decline, weaker immune responses to infections. SIRT1 is important for cell metabolism and immune responses. Researchers pointed out mRNA synthesis and stability which are important factors in the control of gene expression to determine the mechanism of SIRT1 loss during senescence. Knocking out the Atg 7 in senescent cells SIRT1 levels in place indicates the autophagic pathway and not proteasomes which plays a role in the loss of the enzyme. Immunofluorescence staining also showed that LC3 drives the loss of SIRT1 in senescent cells and tissue. A proteasome inhibitor failed to restore SIRT1 protein in senescent cells and tissues while treatment with lys05 rescued its loss.

For determining autophagy ’s role in SIRT1 in immune cells, human donor CD8 T cells were treated with low-dose Lys05 and a proteasome inhibitor and were found that only Lys05 increased SIRT1 levels.

For designing anti-ageing compounds, stabilizing SIRT1 protein level by interrupting the interaction between LC3 and SIRT1 could be a new direction.

Source: Perelman School of Medicine at the University of Pennsylvania

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