They have taken the first step.
A recent study highlighted in Cell Metabolism suggests a potential breakthrough in reversing liver damage associated with aging. Researchers identified a cluster of genes responsible for cell death, specifically through a process called ferroptosis, which is iron-dependent and implicated in various organ damages linked to aging and disease, including the heart, kidneys, and pancreatic tissue.
The study focused on nonalcoholic fatty liver disease (NAFLD), also known as metabolic dysfunction-associated steatotic liver disease (MASLD), a condition that can lead to liver cirrhosis and failure. By analyzing liver cells from aged mice and human samples with NAFLD/MASLD, researchers discovered a genetic signature common across both species, suggesting a potential target for therapeutic intervention.
To test their hypothesis, researchers induced NAFLD/MASLD in young and old mice through diet and administered Ferrostatin-1, a compound known to inhibit ferroptosis, to the older mice. Results showed that liver cells in older mice treated with Ferrostatin-1 exhibited rejuvenated characteristics akin to those of younger, healthier cells.
Senior study author Anna Mae Diehl, MD, emphasized that the research demonstrates aging-related liver damage can be partially reversed, challenging the notion that such damage is irreversible. This finding opens new possibilities for treating NAFLD/MASLD and potentially other age-related organ degenerations by targeting ferroptosis pathways.
Muhammad Nadeem Aslam, MBBS, an assistant research scientist not involved in the study, noted that the study’s findings suggest a shared molecular basis for tissue degeneration across different organs affected by aging and disease. However, he cautioned that while inhibiting ferroptosis could mitigate liver injuries like NAFLD/MASLD, inducing ferroptosis might have therapeutic benefits for conditions such as liver cancer.
NAFLD/MASLD affects approximately one-third of adults globally and is the most common liver disease in children. It is characterized by abnormal accumulation of fat in the liver cells and often lacks noticeable symptoms, making it challenging to diagnose early. Treatment options currently focus on lifestyle changes like diet and exercise to manage the disease’s progression, as there is no direct pharmacological treatment available yet.
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