Scientists successfully revived an ancient gene called uricase, lost by humans millions of years ago, offering a new avenue to tackle gout and related conditions. This gene helps reduce uric acid levels, which are the main culprit behind painful gout attacks and kidney damage.
The team from Georgia State University reconstructed the uricase gene using CRISPR gene editing technology and tested it in engineered human liver cells. The results showed a significant drop in uric acid and fat buildup caused by fructose in the liver cells.
How did scientists revive the uricase gene?
Scientists used genetic data from closely related mammals to reconstruct the uricase gene that human ancestors lost between 20 and 29 million years ago.
Applying CRISPR technology, the gene was reinserted into human liver cells in the lab, restoring the functionality to break down uric acid efficiently.
This gene revival represents not only a technical breakthrough but also a novel way to address diseases linked to excess uric acid in the body, including gout and fatty liver disease.
Did you know?
Humans lost the uricase gene 20 to 29 million years ago, which helped break down uric acid.
What role does uric acid play in gout and other diseases?
Uric acid is a waste product that can form needle-like crystals in joints and kidneys, causing inflammation and pain characteristic of gout. Elevated uric acid levels, known as hyperuricemia, may also contribute to kidney stones, high blood pressure, and cardiovascular diseases.
Because humans lack an active uricase enzyme, uric acid accumulates to harmful levels. Restoring uricase activity could normalize uric acid and reduce the risk of these serious health issues.
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How was the gene editing tested in human cells?
The revived uricase gene was inserted into human liver cells in a laboratory setting. The modified liver cells successfully produced functional uricase enzyme that lowered uric acid and prevented the formation of fatty deposits linked to fructose metabolism.
Further tests in 3D liver spheroids, which mimic liver tissue more closely, confirmed these promising results, indicating potential for future therapeutic use in humans.
What are the potential wider impacts of this therapy?
Beyond gout, lowering uric acid with this gene therapy could help prevent cardiovascular diseases and reduce the risk of kidney-related conditions.
The targeted delivery and activity of uricase in liver cells suggest a precise approach with fewer side effects compared to conventional medicines.
If this therapy proves successful in animal and human trials, it could revolutionize the global management of chronic diseases associated with uric acid.
What challenges remain before this treatment can be used?
Although laboratory results are promising, extensive animal testing and clinical trials are required to confirm safety and efficacy. Researchers also need to ensure that reactivating this ancient gene does not interfere with other vital biological processes.
Accessibility, cost, and large-scale manufacturing are additional considerations before this groundbreaking gene therapy can become widely available to patients.
Looking ahead, this research marks an exciting step toward treatments that harness evolutionary biology and genetic engineering to tackle age-old human diseases effectively.
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