Duke Researchers Uncover Breakthrough to Reverse Liver Aging.

Duke Researchers Uncover Breakthrough to Reverse Liver Aging.

Post by : Elena Malik

In a breakthrough study, researchers at Duke Health have discovered a promising approach to reverse liver aging and combat non-alcoholic liver disease (NAFLD). The liver, resilient as it is, remains vulnerable to damage from various metabolic stresses like high cholesterol, obesity, and diabetes, leading to severe conditions such as cirrhosis and organ failure.

Published in Nature Aging, the study led by Dr. Anna Mae Diehl, explored how aging triggers the death of liver cells and contributes to the progression of metabolic dysfunction-associated steatotic liver disease (MASLD), a widespread condition affecting one in three adults globally.

The research focused on identifying genetic changes in aging livers that drive cell death, particularly through a process known as ferroptosis, which is iron-dependent and exacerbated by metabolic stressors. Analyzing both mouse models and human liver tissues, the team pinpointed specific genetic signatures associated with aging livers and MASLD. These findings provided a clear target for intervention.

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Using an investigational drug called Ferrostatin-1, which inhibits the ferroptosis pathway, researchers conducted experiments on mice fed diets to induce MASLD. Remarkably, mice treated with Ferrostatin-1 showed liver tissues resembling those of young, healthy counterparts, even when subjected to disease-inducing conditions. This outcome suggests a potential therapeutic avenue to rejuvenate liver function in aging and disease-affected individuals.

Dr. Diehl emphasized the broader implications of their findings, noting that blocking ferroptosis could not only benefit liver health but also mitigate damage to other organs affected by MASLD progression. The study underscores the potential for targeted therapies to reverse liver aging and improve outcomes for millions suffering from NAFLD-related conditions worldwide.

July 4, 2024 11:23 a.m. 478

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