Health
New research offers hope for treatment of liver diseases associated with metabolic dysfunction
Fatty liver disease associated with metabolic dysfunction (MASLD) — formerly known as “nonalcoholic liver disease.” fatty liver disease– Approximately 25% of the world's population is affected by its severe form, metabolic dysfunction-associated steatohepatitis (MASH), which can lead to liver fibrosis and liver failure. Currently available approvals There is only one treatment available and it is important to find a solution for MASLD and MASH.
MASLD and MASH are closely related to obesity, inadequate diet, and lack of exercise. These conditions can lead to fat buildup in the liver, causing inflammation and scarring. Over time, it can progress to fibrosis and cirrhosis, which can lead to severe liver damage. Despite the prevalence of MASLD and MASH, there are limited treatment options available to people suffering from MASLD and MASH.
Another problem is reduced levels of a molecule called NAD+ (nicotinamide adenine dinucleotide), which plays a key role in many cellular processes such as energy production, DNA repair, and inflammation control. NAD+ levels decrease in MASLD/MASH, which contributes to liver damage and disease progression. Restoring NAD+ levels may be able to stop or reverse this damage. The question is how.
A team of scientists led by Johan Auwerx at EPFL has shown that inhibiting an enzyme called ACMSD may be the solution. ACMSD (α-amino-β-carboxymuconic acid-ε-semialdehyde decarboxylase) is primarily located in the liver and kidneys and is involved in the breakdown of the amino acid tryptophan and limiting the production of NAD+. Researchers found that blocking ACMSD could increase NAD+ levels in the liver, resulting in reduced inflammation, DNA damage, and fibrosis in a mouse model of MASLD/MASH.
The researchers used several models, including rodent liver cells and human liver organoids (mini-livers grown in the lab). They also fed the mice a fatty Western-style diet to mimic the symptoms that cause MASLD/MASH in humans. Once the mice developed the disease, they administered an ACMSD inhibitor called TLC-065 to the mice and measured its effects on liver function and NAD+ levels in mouse livers, as well as on human liver organoids.
The results were promising. Inhibiting ACMSD significantly increased NAD+ levels, especially in the liver, where ACMSD plays an important role in energy metabolism and protects against DNA damage. This increase in NAD+ reduced inflammation and reversed liver fibrosis and DNA damage in treated mice. However, they also found that inhibiting ACMSD in human liver organoids also reduced markers of DNA damage.
The results of this study indicate that blocking ACMSD may represent a new treatment for MASLD and MASH. Promoting NAD+ production in the liver may protect against the severe damage caused by these diseases and reduce the likelihood of progression to cirrhosis. This approach also highlights the importance of metabolic pathways in liver diseases and provides ACMSD as a new target for drug development.
other contributors
- Cincinnati Children's Hospital Medical Center (CCHMC)
- Amsterdam UMC
- University of Lausanne
- Ortho Bio Co., Ltd.
- Osaka University
funding
- EPFL
- European Research Council
- Swiss National Science Foundation (SNSF)
- synergistic effect
- National Research Foundation of Korea (NRF)
- European Molecular Biology Organization (EMBO)
- bright focus
- European Union's Horizon Europe research and innovation program
- MSCA-Doctor Network
- National Institutes of Health
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Reference magazines:
Ryu, Y.J. Others. (2024). ACMSD inhibition corrects fibrosis, inflammation, and DNA damage in MASLD/MASH. hepatology journal. doi.org/10.1016/j.jhep.2024.08.009.
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