Scientists at UCLA have uncovered a medical breakthrough that could be a potential miracle for millions of Los Angeles residents.
The Westwood university released a study that reveals a way to reverse chronic fatty liver disease without a major change in one’s diet.
It is estimated that between 30% and 40% of Los Angeles residents (between 2.8 million and 3.8 million people) have fatty liver disease, which is especially prevalent in the Latino communities.
The current treatments for fatty liver disease are quite limited and often demand invasive methods, but that could change with these new findings.
“This is a huge public health crisis in the making,” said Anthony Covarrubias, the senior author of the study and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.
“We’re seeing fatty liver disease in younger and younger people. So we’re really happy to make some inroads into understanding what’s driving it and identifying cell types we might be able to target,” Covarrubias added.
The researchers discovered a “rogue group of immune cells” that they believe are the driving factors in chronic liver disease.
These “zombie cells” appear to drive inflammation in the liver, and when the scientists removed them in a group of mice, the results were astonishing.
The liver damage not only improved but was completely reversed, even though the mice continued eating an unhealthy diet.
The study focused on “cellular senescence,” a process that occurs when cells stop dividing but do not die, and when they remain in tissues, they can cause damage to healthy neighboring cells.
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“Senescent cells are fairly rare, but think of them like a broken-down car on the 405,” Covarrubias added.
“Just one stalled car can back up traffic for miles. Now imagine five or ten of them slowly accumulating. That’s what these cells do to a tissue: even a small number causes enormous disruption.”
These “zombie cells” will develop with age, with researchers finding them in just 5% of younger mice and a whopping 60-80% in older mice.
While age is a driving factor for these cells emerging, high cholesterol levels can push healthy macrophages — the larger immune cells that clear out unhealthy or dead cells — into a senescent state.
“Physiologically, macrophages can handle cholesterol metabolism,” said Ivan Salladay-Perez, first author of the new study and a graduate student.
“But in a chronic state, it’s pathological. And when you look at fatty liver disease, which is driven by overnutrition and too much cholesterol in the blood, that excess cholesterol appears to be a major driver of the senescent macrophage population.”
The research team is now working to identify drugs that will be able to remove senescent macrophages without any side effects.
