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Anti-aging molecule could improve liver and kidney treatments
Scientists have revealed that an enzyme that is present in the liver and kidneys limits the activity of a molecule that plays a role in cell metabolism and longevity. Their research suggests that blocking this enzyme could be a way to preserve the health of these organs.
Nicotinamide adenine dinucleotide (NAD+) is called the “anti-aging molecule” because research has shown that its levels fall with age and that restoring them can extend years of good health and even longevity itself.
This molecule plays a key role in several biological processes that help cells get energy and stay healthy, such as metabolism, DNA repair, gene expression, and cell signaling
Scientists class NAD+ as a coenzyme, meaning that it does not act alone but helps the enzymes that drive these vital cell processes.
One family of enzymes that NAD+ has an ancient “intimate connection” with is the sirtuins.
Studies have shown that as NAD+ declines with age, it reduces sirtuin activity in ways that affect the communication between the cell nucleus and its mitochondria, which are the tiny compartments that produce energy for the cell.
Control of NAD+ is ‘evolutionarily conserved’
A recent study by the Medical Association is published in a scientific journal. It demonstrates two compounds that can restore fallen NAD + levels in the liver and kidneys.
Cells synthesize NAD + from scratch using the amino acid tryptophan as a basic building block.
This “de novo synthesis” requires the presence of certain enzymes, including one called aminocarboxymuconate-semialdehyde decarboxylase (ACMSD), which has the effect of limiting the production of NAD+.
The team describes the way in which ACMSD controls NAD+ levels in cells as being “evolutionarily conserved.”
Their investigation demonstrated that the mechanism was the same in both Caenorhabditis elegans, a type of worm, and mice and that blocking ACMSD increased both NAD+ and mitochondrial activity.
Selective ACMSD inhibitors
The researchers discovered that blocking ACMSD also raised the activity of one of the sirtuins that NAD+ works with. The combination of elevated sirtuin activity and increased NAD+ synthesis boosted mitochondrial activity.
Working with TES Pharma, the team then tested the effect of two selective ACMSD blockers in animal models of nonalcoholic fatty liver disease and kidney damage. Both compounds seemed to “preserve” liver and kidney function.
Since the enzyme is mainly found in the kidneys and liver, the ability of ACMSD inhibitors to protect these organs from damage has been tested.
As ACMSD does not occur elsewhere in the body, the finding could pave the way for a protective treatment that boosts NAD+ without affecting other organs.