Publications by authors named "B Pintado"
Article Synopsis
- Accumulation of lipid-laden macrophages is vital in forming atherosclerotic plaques, and reduced ZEB1 levels in these cells lead to larger plaques and increased cardiovascular risk.
- Male mice lacking ZEB1 in myeloid cells show significant lipid build-up and metabolic issues, indicating that ZEB1 deficiency worsens atherosclerosis.
- Targeted delivery of ZEB1 using nanoparticles can reverse lipid accumulation and reduce plaque formation, suggesting that ZEB1 could be an important therapeutic target for atherosclerosis.
Acute inflammation can either resolve through immunosuppression or persist, leading to chronic inflammation. These transitions are driven by distinct molecular and metabolic reprogramming of immune cells. The anti-diabetic drug Metformin inhibits acute and chronic inflammation through mechanisms still not fully understood.
View Article and Find Full Text PDFReactive oxygen species (ROS) serve important homeostatic functions but must be constantly neutralized by an adaptive antioxidant response to prevent supraphysiological levels of ROS from causing oxidative damage to cellular components. Here, we report that the cellular plasticity transcription factors ZEB1 and ZEB2 modulate in opposing directions the adaptive antioxidant response to fasting in skeletal muscle. Using transgenic mice in which or were specifically deleted in skeletal myofibers, we show that in fasted mice, the deletion of , but not , increased ROS production and that the adaptive antioxidant response to fasting essentially requires ZEB1 and is inhibited by ZEB2.
View Article and Find Full Text PDFBackground: A recent trial showed that management driven by prognostic assessment was effective in reducing the length of stay (LOS) for acute stable pulmonary embolism (PE). The efficacy and safety of this strategy in each subgroup of risk stratification remains unknown.
Methods: We conducted a analysis of the randomized IPEP study to evaluate the effect of a management strategy guided by early use of a prognostic pathway in the low- and intermediate-high risk subgroups defined by the European Society of Cardiology (ESC) model.