A paper by Kwangwon Lee, Ph.D., and a team of NEOMED researchers in the lab of Takhar Kasumov, Ph.D., has been peer reviewed and accepted in Molecular & Cellular Proteomics, a prestigious journal that reports significant novel biological or clinical discoveries underpinned by proteomic observations across all kingdoms of life.
In this paper, the authors investigated the mechanisms of initiation and progression of nonalcoholic fatty liver disease (NAFLD), a disease that affects more than 30 percent of the U.S. population. The disease ranges from steatosis (fat accumulation in the liver) to nonalcoholic steatohepatitis (NASH). It can lead to cirrhosis and hepatocarcinoma. While steatosis can be treated with lifestyle modification, there is currently no established therapy for NASH. This is because the mechanisms of the disease progression from steatosis to NASH are not fully understood. In the paper, the investigators report their findings on the role of mitochondrial dysfunction in this process.
The authors used a state-of-art proteomics approach and found that hepatic oxidative stress resulted in enhanced degradation of mitochondrial proteins involved in energy production in a diet-induced mouse model of NAFLD. To remove the damaged mitochondria, cells from fatty livers digested their mitochondria more, through a process known as mitophagy, but did not increase production of mitochondria. According to the author’s findings, this resulted in lower mitochondrial copy number and ATP level in the liver cells of mice with NAFLD.
This paper was highlighted in the ASBMB Today, an ASMB member magazine; and in an online press release.
View the abstract at Molecular & Cellular Proteomics.
The study was supported by NIH grant funding and NEOMED. Dr. Kasumov is an assistant professor of pharmaceutical sciences. His lab is part of NEOMED’s Neurodegenerative Disease and Aging and the Diabetes, Obesity and Metabolism Research focus areas.