A new study shows that humans express a powerful hormone during exercise and that treating mice with the hormone improves physical performance, capacity and fitness. Researchers say the findings present new possibilities for addressing age-related physical decline.

The research, published on Wednesday in Nature Communications, reveals a detailed look at how the mitochondrial genome encodes instructions for regulating physical capacity, performance and metabolism during aging and may be able to increase healthy lifespan.

“Mitochondria are known as the cell’s energy source, but they are also hubs that coordinate and fine-tune metabolism by actively communicating to the rest of the body,” said Changhan David Lee, assistant professor at the USC Leonard Davis School of Gerontology and corresponding author of the study. “As we age, that communication network seems to break down, but our study suggests you can restore that network or rejuvenate an older mouse so it is as fit as a younger one.”

Scientists in Beijing may be one step closer to having the answer to living longer and reversing the effects of ageing. A group of biologists at the Chinese Academy of Sciences say they have developed a world-first new gene therapy and have been running tests on mice. It involved screening around 10000 genes in search of particularly strong drivers of cellular ageing. They identified 100 genes in that pool, but the one that really stood out was the kat7. They then inactivated that kat7 gene in the livers of mice, Professor Qu Jing explained some of their findings: “These mice show after six to eight months, they show overall improved appearance and grip strength and most importantly they have extended lifespan for about 25%.” Kat7 is one of tens of thousands of genes found in the cells of mammals. The scientists also tested the function of the gene in human stem cells, human liver cells and more. So far there have been no side effects of cellular toxicity. Despite this, the method still has a long way to go from being ready for human trials and will require a lot of funding and much more research. “In the end we do hope that we can find a way to delay ageing even by a very minor percentage we want to delay the human ageing in the future.” For now, there’s no final answer to cheating death, but the scientists plan on testing the function of kat7 in other cell types of humans and other organs of mice.

NRF2 is just one of thousands of critical proteins in the cell, but it is one that we now know a lot about. Once any molecule achieves a certain level of celebrity status, it tends to acquire a groupie following in the supplement market. Today, we have all manner of NRF enhancers, releasers, activators and synergizers ready to arrive on your doorstep at the click of a button. But what could any of these things possibly do for us, and how much is too much of a good thing?

At the risk of overstating the obvious, if a little extra NRF2 is good for every cell in your body, and every cell in your body is good, then NRF2 must be good for your body. The weak link in that argument, however, is that all cells are not good. Nobody wants harmful bacterial cells to flourish, and nobody wants cancer cells to flourish. A paper recently published in Nature now suggests that inhibiting NRF2 can block the migration and invasion of non-small-cell lung cancer cells through the body. If anyone is going to derive benefit from NRF2, they may need to be smart about it.

The main reason NRF2, or Nuclear factor-erythroid 2-related factor 2, is so highly sought, is because it is a key transcriptional regulator of several antioxidant and anti-inflammatory enzymes. Unfortunately, as the authors above have revealed, it also moonlights as an activator of the Rho-ROCK pathway, which promotes actin filamentation and movement of cells. The researchers were able to block this activity of NRF2 by giving an inhibitor known as brusatol.