Publications by authors named "J C Fernandez-Checa"
Article Synopsis
- - Cholestatic liver diseases (CLD) cause damage to the liver cells and can lead to fibrosis and cirrhosis due to bile acid accumulation, with STARD1 playing a potential role in this process.
- - Research found that patients with primary biliary cholangitis had higher STARD1 levels, and mice lacking STARD1 specifically in liver cells were more resistant to liver damage and inflammation associated with bile duct blockage.
- - The study suggests that targeting STARD1 could be a promising approach for treating cholestatic liver injury, as it appears to influence bile acid levels and oxidative stress in liver cells.
Background & Aims: In patients with cirrhosis, acute decompensation (AD) correlates with a hyperinflammatory state driven by mitochondrial dysfunction, which is a significant factor in the progression toward acute-on-chronic liver failure (ACLF). Elevated circulating levels of acylcarnitine, indicative of mitochondrial dysfunction, are predictors of mortality in ACLF patients. Our hypothesis posits that acylcarnitines not only act as biomarkers, but also actively exert detrimental effects on circulating immune cells.
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- Alcohol-associated liver disease (ALD) is a major cause of chronic liver disease, leading to serious conditions like cirrhosis and liver cancer due to the harmful effects of alcohol metabolism.
- The complexity of ALD's pathology has hindered drug development, highlighting the need for better understanding of its underlying mechanisms.
- Mitochondria play a key role in ALD progression, so studying their function may uncover new treatment strategies for this disease.
Background And Objectives: Fibrosis contributes to 45% of deaths in industrialized nations and is characterized by an abnormal accumulation of extracellular matrix (ECM). There are no specific anti-fibrotic treatments for liver fibrosis, and previous unsuccessful attempts at drug development have focused on preventing ECM deposition. Because liver fibrosis is largely acknowledged to be reversible, regulating fibrosis resolution could offer novel therapeutical options.
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