Publications by authors named "F Perocchi"
The mitochondrial calcium uniporter channel (MCUC) mediates mitochondrial calcium entry, regulating energy metabolism and cell death. Although several MCUC components have been identified, the molecular basis of mitochondrial calcium signaling networks and their remodeling upon changes in uniporter activity have not been assessed. Here, we map the MCUC interactome under resting conditions and upon chronic loss or gain of mitochondrial calcium uptake.
View Article and Find Full Text PDFEndothelial cells (ECs) are highly plastic, capable of differentiating into various cell types. Endothelial-to-mesenchymal transition (EndMT) is crucial during embryonic development and contributes substantially to vascular dysfunction in many cardiovascular diseases (CVDs). While targeting EndMT holds therapeutic promise, understanding its mechanisms and modulating its pathways remain challenging.
View Article and Find Full Text PDFLipid composition is conserved within sub-cellular compartments to maintain cell function. Lipidomic analyses of liver, muscle, white and brown adipose tissue (BAT) mitochondria revealed substantial differences in their glycerophospholipid (GPL) and free cholesterol (FC) contents. The GPL to FC ratio was 50-fold higher in brown than white adipose tissue mitochondria.
View Article and Find Full Text PDFArticle Synopsis
- Brown adipose tissue (BAT) helps maintain body temperature in cold environments through a protein called UCP1, but the evolutionary origins of this process are not well understood.
- Research indicates that marsupials have a nonthermogenic variant of UCP1, suggesting a different evolutionary pathway compared to eutherian mammals (like humans), which developed a thermogenic form of UCP1.
- The findings imply that mammalian BAT thermogenesis evolved in two stages: an initial nonthermogenic stage in the common ancestor of therian mammals and later the development of thermogenic capabilities specifically in eutherians after their divergence from marsupials.
Article Synopsis
- * Research shows that neuroinflammatory lesions in mouse spinal cords lead to significant energy deficits in axons, impacting mitochondrial performance and enzyme levels in the tricarboxylic acid (TCA) cycle.
- * Enhancing the expression of specific TCA cycle enzymes can help restore energy balance in affected neurons, indicating a potential therapeutic target for treating energy deficiencies in MS.