Publications by authors named "U Nogueira-Recalde"
Article Synopsis
- ACBP/DBI is a protein linked to metabolic-associated steatohepatitis and liver fibrosis, showing higher levels in affected patients, correlating strongly with NAFLD and FIB4 scores, regardless of age or body mass index.
- A study used a monoclonal antibody to neutralize ACBP/DBI in various mouse models of liver disease, resulting in reduced signs of liver damage and halting disease progression.
- The results suggest ACBP/DBI plays a causal role in liver conditions and could be a potential therapeutic target for treating liver diseases.
Article Synopsis
- Higher plasma levels of ACBP/DBI, linked to age and obesity, are associated with an increased risk of cancer, especially in patients with genetic predispositions like BRCA1/2 or TP53 mutations.
- In studies, elevated ACBP/DBI levels were predictive of future cancer development, particularly lung cancer, while neutralization of ACBP/DBI slowed tumor growth and enhanced the effects of chemoimmunotherapy in animal models.
- The research suggests that ACBP/DBI functions as an immune suppressor and indicates that targeting it may improve cancer immunotherapy outcomes.
Extracellular acyl-coenzyme A binding protein [ACBP encoded by diazepam binding inhibitor (DBI)] is a phylogenetically ancient appetite stimulator that is secreted in a nonconventional, autophagy-dependent fashion. Here, we show that low ACBP/DBI plasma concentrations are associated with poor prognosis in patients with anorexia nervosa, a frequent and often intractable eating disorder. In mice, anorexia induced by chronic restraint stress (CRS) is accompanied by a reduction in circulating ACBP/DBI concentrations.
View Article and Find Full Text PDFAuthors have demonstrated that apoptosis activation is a pathway related to cartilage degradation characteristics of the OA process. Autophagy is an adaptive response to protect cells from various environmental changes, and defects in autophagy are linked to cell death. In this sense, decreased autophagy of chondrocytes has been observed in OA articular cartilage.
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