Mutations in key proteins of autophagy extend healthy lifespan of mice

  Autophagy is an evolutionarily conserved protein degradation pathway—eliminating dysfunctional cellular components and recycling their components. It helps to extend the lifespan of model organisms; however, it still plays a role in mammalian lifespan. Little known.

  Beth Levine and colleagues at the University of Texas Southwestern Medical Center have previously shown that specific mutations in the protein beclin1 increase autophagy in the brain and muscle of mice, and also increase the performance of mouse models of Alzheimer’s disease. Cognitive function. Now, they report that these mice not only live longer, they also live longer healthy lives because of the reduction in various aging-related phenotypes (such as heart disease and kidney disease and tumor development). The same beclin1 mutation can also solve the problem of early death and infertility in mice caused by insufficient anti-aging protein klotho.

  The authors concluded that this mutation works by releasing beclin1 from negative regulators, and may be an effective mechanism for mammals to increase autophagy, prevent premature aging, and extend healthy and longevity.