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Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure
TLDR
Temporary administration of PA inhibitor-1 or the matrix metalloproteinase-inhibitor TIMP-1 completely protected wild-type mice against rupture but did not abort infarct healing, thus constituting a new approach to prevent cardiac rupture after acute myocardial infarction. Expand
Fatty acid carbon is essential for dNTP synthesis in endothelial cells
TLDR
It is reported that endothelial loss of CPT1A, a rate-limiting enzyme of fatty acid oxidation (FAO), causes vascular sprouting defects due to impaired proliferation, not migration, of human and murine endothelial cells. Expand
Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism
TLDR
It is shown that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparα pathway. Expand
A mouse model for Zellweger syndrome
TLDR
Analysis of the neocortex revealed impaired neuronal migration and maturation and extensive apoptotic death of neurons in the cerebro-hepato-renal syndrome of Zellweger mice. Expand
Identification and Characterization of the Putative Human Peroxisomal C-terminal Targeting Signal Import Receptor (*)
TLDR
All available evidence indicates that the PTS1-binding protein is part of the peroxisomal protein import machinery and most probably is the long sought after human PTS1 import receptor. Expand
Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation
TLDR
Analysis of atherosclerotic aorta in mice with a deficiency of apoliprotein E indicated that deficiency of u-PA protected against media destruction and aneurysm formation, probably by means of reduced plasmin-dependent activation of pro-MMPs. Expand
Oxygen sensors at the crossroad of metabolism.
TLDR
A "metabolo-centric" overview of the role of the PHD/FIH members of this family in metabolism on how they regulate O( 2) supply and consumption, energy compensation and conservation, O(2) conformance and hypoxia tolerance, redox and pH homeostasis, and other vital metabolic processes with implications in health and disease. Expand
Axonal loss and neuroinflammation caused by peroxisome-deficient oligodendrocytes
TLDR
It is concluded that peroxisomes provide oligodendrocytes with an essential neuroprotective function against axon degeneration and neuroinflammation, which is relevant for human demyelinating diseases. Expand
Mitochondrial alterations caused by defective peroxisomal biogenesis in a mouse model for Zellweger syndrome (PEX5 knockout mouse).
TLDR
Evidence is presented that the absence of functional peroxisomes, causing a general defect inPeroxisomal metabolism, leads to proliferation of pleomorphic mitochondria with severe alterations of the mitochondrial ultrastructure, changes in the expression and activities of mitochondrial respiratory chain complexes, and an increase in the heterogeneity of the mitochondria compartment in various organs and specific cell types. Expand
Inactivation of the Peroxisomal Multifunctional Protein-2 in Mice Impedes the Degradation of Not Only 2-Methyl-branched Fatty Acids and Bile Acid Intermediates but Also of Very Long Chain Fatty Acids*
TLDR
The present data indicate that MFP-2 is not only essential for the degradation of 2-methyl-branched fatty acids and the bile acid intermediates di- and trihydroxycoprostanic acid but also for the breakdown of very long chain fatty acids. Expand
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