The Interplay Between Cellular Senescence And Lipid Metabolism In The Progression Of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
Our livers are vital organs, and a growing concern worldwide is a condition called metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease. This condition can range from simple fat accumulation in the liver to more severe inflammation and damage, potentially leading to serious complications like fibrosis and even liver cancer.
Recent research highlights two key players in the worsening of this disease: cellular senescence and lipid droplets. Cellular senescence refers to cells that have stopped dividing but remain active, accumulating in tissues and potentially causing harm. Lipid droplets are essentially tiny storage units for fat within cells.
The study explains that senescent liver cells undergo significant changes in how they handle fats, often increasing their uptake of lipids. Initially, the liver might try to counteract this by boosting its fat-burning processes. However, if these senescent cells persist, they can lead to problems with the cell’s energy-producing factories, called mitochondria, and further suppress the liver’s ability to burn fat.
Furthermore, these senescent cells release a cocktail of inflammatory signals, known as the senescence-associated secretory phenotype (SASP), which fuels chronic inflammation in the liver. Interestingly, the paper suggests that lipid droplets are not just passive storage units but actively influence these senescence-related signals. Understanding and potentially disrupting this intricate communication between cellular senescence and lipid regulation could open new avenues for treating MASLD and preventing its progression.
Source: link to paper