{"id":3828,"date":"2025-12-01T17:56:48","date_gmt":"2025-12-01T17:56:48","guid":{"rendered":"https:\/\/magazines.uthscsa.edu\/schools\/?p=3828"},"modified":"2025-12-03T17:09:04","modified_gmt":"2025-12-03T17:09:04","slug":"bold-research-aims-to-halt-liver-disease-before-it-turns-deadly","status":"publish","type":"post","link":"https:\/\/magazines.uthscsa.edu\/schools\/2025\/12\/01\/bold-research-aims-to-halt-liver-disease-before-it-turns-deadly\/","title":{"rendered":"Bold research aims to halt liver disease before it turns deadly"},"content":{"rendered":"

By Claire Kowalick<\/p>\n

Metabolic dysfunction-associated steatotic liver disease, or MASLD, is the most common form of steatotic liver disease marked by fat accumulation in the liver. Formerly known as NASLD, or non-alcoholic steatotic liver disease, or fatty liver, the new terminology marks scientists’ deeper understanding of underlying mechanisms of the disease.<\/p>\n

In many MASLD cases, liver fat accumulation is linked to obesity, Type 2 diabetes and insulin resistance. While MASLD may begin silently enough, like a smoldering fire, it can combust into a far more dangerous condition.<\/p>\n

Fat to fibrosis: A dangerous turn<\/strong><\/span><\/h3>\n

In early stages, MASLD may not cause problems and is potentially reversible. However, when chronic liver fat accumulation leads to inflammation and damage to liver cells, MASLD turns into MASH, or metabolic dysfunction-associated steatohepatitis. MASH can cause inflammation, enlarged liver and fibrosis, or scarring. Over time, this can progress to cirrhosis, liver failure and potentially liver cancer. Most people with MASH do not experience symptoms until an advanced stage of the disease when pain, jaundice and fluid retention begin to appear.<\/p>\n

\u201cThe liver can take a lot of abuse,\u201d said Luke Norton, PhD, director of the Center for Molecular Metabolism and assistant professor in the Department of Medicine at the Joe R. and Teresa Lozano Long School of Medicine at The University of Texas at San Antonio. \u201cBut once fibrosis sets in, it becomes incredibly difficult to reverse.\u201d<\/p>\n

\u2018Perfect storm\u2019 of risk in San Antonio<\/span><\/strong><\/h3>\n

In the South Texas area, MASLD and MASH are alarmingly common. Norton said up to 90% of people with obesity also have MASLD. Among patients with Type 2 diabetes in San Antonio, nearly 60% have MASLD, and studies indicate up to 30% also have MASH.<\/p>\n

This startling trend is not limited to adults. Pediatric MASH cases are on the rise as well, with San Antonio physicians reporting diagnoses in children as young as 8 years old.<\/p>\n

How do you diagnose a disease with no symptoms?<\/span><\/strong><\/h3>\n

Early detection is critical but can be difficult due to a lack of diagnostic tools. The most accurate MASH diagnosis requires liver biopsy to confirm inflammation and fibrosis. Imaging tools like FibroScan \u2014 a specialized ultrasound that estimates liver stiffness and fat \u2014 and MRI-based techniques offer non-invasive alternatives, but they are not widely available in most primary care settings.<\/p>\n

\u201cBy the time most people are diagnosed, the disease has progressed,\u201d Norton said. \u201cWe need broader screening and education, especially in communities with high obesity and diabetes rates.\u201d<\/p>\n

\"\"\u201cBy the time most people are diagnosed, the disease has progressed. We need broader screening and education, especially in communities with high obesity and diabetes rates.\u201d<\/span><\/p><\/blockquote>\n

\u2013 Luke Norton, PhD,<\/strong> director of the Center for Molecular Metabolism and assistant professor in the Department of Medicine<\/span><\/h5>\n

Why liver fat matters<\/strong><\/span><\/h3>\n

Beyond its actions on the liver itself, liver fat can be a sign of more wide-ranging metabolic dysfunction. Insulin resistance makes fat cells less responsive to storing glucose and lipids, and instead of storing these excess energy molecules, they begin dumping them into the bloodstream. The liver then becomes a catchall, taking in the excess fat. Once the liver can\u2019t take any more, it triggers inflammation, impairs detoxification and throws off glucose metabolism.<\/p>\n

\u201cPeople think of fat as just being stored away,\u201d Norton said. \u201cBut when it goes to the wrong places, like the liver, it starts actively doing harm.\u201d<\/p>\n

Treatments and the role of obesity<\/strong><\/span><\/h3>\n

While there are few U.S. Food and Drug Administrationapproved medications specifically for MASLD or MASH, several drugs are showing promise in prevention and slowing of progression of the diseases. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), already used for Type 2 diabetes and obesity, can also help reduce liver fat. Pioglitazone, an insulin sensitizer and Type 2 diabetes drug, reduces blood sugar and may also potentially slow liver fibrosis.<\/p>\n

The most powerful MASLD preventive measures include lifestyle interventions like exercise, a balanced low-carbohydrate, low-sugar diet and little, if any, alcohol. If caught early, Norton said these changes in diet, physical activity and weight management can make a difference.<\/p>\n

\"\"\u201c Magnesium is a core ion. It is the first ion used by living organisms. Without it, ATP, the energy molecule in every cell, is unstable and inflammatory. Magnesium binds ATP, stabilizes it, and makes it usable. But when magnesium floods the mitochondria, the whole system gets thrown off.\u201d<\/span><\/p><\/blockquote>\n

\u2013 Madesh Muniswamy, MS, PhD<\/strong>, Long-Endowed tenured professor of medicine in the Division of Cardiology<\/span><\/h5>\n

\"\"Deep dive: Reprogramming <\/span>at the molecular level<\/span><\/strong><\/h3>\n

Understanding how liver disease first develops requires looking down to the mitochondrial level. For decades, Madesh Muniswamy, MS, PhD, professor of medicine at the Long School of Medicine\u2019s Division of Cardiology, has studied mitochondrial metabolism, or how bodies convert sugar and fat into energy.<\/p>\n

\u201cOur lab is trying to understand why, at the cellular level, some people store everything they eat as fat, while others do not,\u201d he said. Muniswamy\u2019s lab, in collaboration with other institutions, has identified a crucial gene involved in a specific mitochondrial ion channel that regulates magnesium.<\/p>\n

\u201cMagnesium is a core ion. It is the first ion used by living organisms,\u201d he said. \u201cWithout it, ATP, the energy molecule in every cell, is unstable and inflammatory. Magnesium binds ATP, stabilizes it and makes it usable. But when magnesium floods the mitochondria, the whole system gets thrown off.\u201d<\/p>\n

Using mouse models and human biobank samples, the team has shown that in people genetically predisposed to obesity, the mitochondrial magnesium channel is overactive and pulls excess magnesium into the mitochondria. This slows the burning of sugar and fat, and instead of being used for energy, nutrients are stored as fat across the body, including the liver. Over time, this accumulation reshapes the entire metabolic profile, essentially reprogramming the body to store fat rather than burn it.<\/p>\n

This buildup can lead to MASLD, MASH and potentially liver cancer. In a one-year study \u2014 equivalent to 40 years in human life \u2014 mice lacking this magnesium channel gene that were fed a Western high-fat, high-carbohydrate diet quickly developed MASH and liver tumors.<\/p>\n

\u201cDietary stress is driving this. In our studies, mouse models of obesity show an 80% decrease in mitochondrial number and function in liver cells,\u201d Muniswamy said. \u201cWhen that happens, there is nothing left to burn fat or sugar, and fat builds up.\u201d<\/p>\n

Muniswamy and his team have patented the discovery, launched a biotech company and are now focused on designing a drug that can partially close this channel, which would slow magnesium entry while allowing calcium to get through. Calcium, unlike magnesium, turns on the energy-burning pathways in the cell.<\/p>\n

\"\"\u201cBy eliminating senescent cells, we saw dramatic improvements in liver structure and function. This gives us real hope for a new class of therapeutics.\u201d<\/span><\/p><\/blockquote>\n

\u2013 Daohong Zhou, MD,<\/strong> tenured professor in the Department of Biochemistry and Structural Biology, director of the Target Discovery Core at the Greehey Children\u2019s Cancer Research Institute, associate director for drug development at the Mays Cancer Center and director of the Center for Innovative Drug Discovery<\/span><\/h6>\n

Novel treatments bring new hope<\/span><\/strong><\/h3>\n

As Health Science Center scientists uncover the complexities of metabolic-related liver disease, many also seek to understand how chronic liver damage from these diseases can lead to liver cancer. A growing number of studies suggest that chronic metabolic damage related to obesity and Type 2 diabetes can lead to hepatocellular carcinoma (HCC), the most common form of liver cancer. However, some surprising discoveries and a bold new treatment have paved the way for treatments that stop the disease progression, potentially halting cancer progression.<\/p>\n

\u201cOnce fibrosis reaches a certain stage, it becomes a self-propagating disease, and current treatments cannot reverse it effectively,\u201d said Daohong Zhou, MD, tenured professor in the Long School of Medicine\u2019s Department of Biochemistry and Structural Biology. He is also director of the university\u2019s Target Discovery Core at the Greehey Children\u2019s Cancer Research Institute, associate director for drug development at the Mays Cancer Center and director of the Center for Innovative Drug Discovery.<\/p>\n

Zhou\u2019s research seeks to understand the role of senescent cells in this progression to cancer. These aged, non-dividing cells accumulate in damaged tissue and secrete molecules that promote inflammation and disrupt normal healing in the liver. His lab has found that clearing these cells using targeted senolytic agents in mouse models of liver fibrosis not only reduces inflammation and halts fibrotic progression but may also prevent liver cancer altogether.<\/p>\n

\u201cBy eliminating senescent cells, we saw dramatic improvements in liver structure and function,\u201d Zhou said. \u201cThis gives us real hope for a new class of therapeutics.\u201d<\/p>\n

Unlike earlier, broad-spectrum senolytics, the new agents Zhou is developing are more refined and designed to clear only harmful senescent cells in specific organs while preserving their beneficial functions elsewhere in the body.<\/p>\n

\u201cSome senescent cells are useful,\u201d Zhou said. \u201cThat\u2019s why we believe in developing senolytic drugs that only work in diseased tissue.\u201d<\/p>\n

This kind of precision therapy is crucial for complex organs like the liver, which must continue performing vital metabolic tasks even when compromised by disease.<\/p>\n

\u201cIt\u2019s always better to prevent than to treat late-stage disease,\u201d Zhou said. \u201cIf we can reverse MASH or slow fibrosis, we may be able to stop liver cancer before it starts.\u201d<\/p>\n

His lab is now exploring combination therapies, such as pairing senolytic agents with metabolic drugs to maximize their protective effects.<\/p>\n

\"\"\u201cWe\u2019re using single-cell RNA sequencing to understand how tumor cells express different genes and how those influence their immune environment,\u201d Sun said. \u201cThe hope is to identify molecular signatures that not only predict treatment response but can also be targeted to make \u2018cold\u2019 tumors responsive.\u201d<\/span><\/p><\/blockquote>\n

\u2013 LuZhe Sun, PhD<\/strong>, professor and Dielmann chair in oncology in the Department of Cell Systems and Anatomy and associate director for shared resources at the Mays Cancer Center<\/span><\/h6>\n

Progress in immunotherapy<\/strong><\/span><\/h3>\n

While prevention is best, many patients are diagnosed with liver cancer after it has already started proliferating. That\u2019s where LuZhe Sun, PhD, and his team come in. Sun is professor and Dielmann chair in oncology in the Department of Cell Systems and Anatomy at the Long School of Medicine and associate director for shared resources at the Mays Cancer Center. He seeks to develop therapies that treat HCC and overcome resistance to current treatments.<\/p>\n

One major challenge with HCC is the variable response to immunotherapy, including immune checkpoint inhibitors (ICI) such as pembrolizumab or atezolizumab that are common frontline treatments. Sun\u2019s lab has developed mouse models of advanced liver cancer that mimic the way tumors develop in the human body. This allows him to test which tumors are immune \u201chot,\u201d and likely respond well to ICI treatment, and which are immune \u201ccold,\u201d meaning they respond less or do not respond at all.<\/p>\n

\u201cWe\u2019re using single-cell RNA sequencing to understand how tumor cells express different genes and how those influence their immune environment,\u201d Sun said. \u201cThe hope is to identify molecular signatures that not only predict treatment response but can also be targeted to make \u2018cold\u2019 tumors responsive.\u201d<\/p>\n

His lab is also exploring gene targets involved in fibrosis and tumor progression, including STEAP2, a protein that promotes liver copper uptake and activates proliferative signaling pathways. In collaboration with other university scientists, Sun is developing novel inhibitors that may help prevent fibrosis or even allow some reversal of liver scarring.<\/p>\n

\u201cIf fibrosis is dynamic, meaning the fibers are constantly being built and broken down, then blocking that enzyme function could shift the balance toward healing,\u201d said Sun.<\/p>\n

Along with these efforts, his team is also investigating combinations of cell-cycle inhibitors and the mTOR inhibitor rapamycin, which have shown encouraging results in early studies.<\/p>\n

\u201cWe\u2019ve seen good responses in \u2018hot\u2019 tumor models, and the next step is to test their effectiveness in \u2018cold\u2019 tumors,\u201d he said.<\/p>\n

Progress in liver cancer treatment centers on understanding not just the disease, but also the liver\u2019s unique biology. Unlike other organs, the liver metabolizes most drugs, complicating the use of many traditional cancer therapeutics.<\/p>\n

\u201cThat\u2019s why many chemotherapeutic agents are not used for liver cancer,\u201d said Sun. \u201cAny new drug must strike a delicate balance by being powerful against tumors but gentle on normal liver function.\u201d<\/p>\n

A better mechanistic understanding of liver disease and cancer, early intervention and targeted therapies could mean a future where liver cancer is no longer a dreaded diagnosis but a preventable, manageable condition.<\/p>\n

\u201cLiver disease is complex,\u201d Sun said. \u201cBut with new tools, new understanding and a collaborative approach, we are closer than ever to real solutions.\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"

Researchers, including Dr. Luke Norton and Dr. Madesh Muniswamy, are leading efforts to understand and prevent metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (MASH).<\/p>\n","protected":false},"author":653,"featured_media":3829,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[11,12],"magazine":[22],"issue-year":[59],"featured-story":[36,37],"class_list":["post-3828","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-patient-care","category-research","magazine-future","issue-year-59","featured-story-homepage","featured-story-landing-page"],"yoast_head":"\nBold research aims to halt liver disease before it turns deadly - Magazines of the Schools at UT Health San Antonio<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/magazines.uthscsa.edu\/schools\/2025\/12\/01\/bold-research-aims-to-halt-liver-disease-before-it-turns-deadly\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Bold research aims to halt liver disease before it turns deadly - 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