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Stress signals, such as UV radiation or ROS themselves, activate p66Shc, which was proposed to stimulate its H2O2 forming activity, ultimately triggering mitochondrial disintegration.
Poly- ADP-ribose) Poly- ADP-riboseRPoly- ADP-ribosethat was recently shown to mediate mitochondrial disintegration and cell death after oxidative stress.
Although the respective enzyme, HSD10 has an important role in mitochondrial metabolism, we show that the adverse effects of its deficiency are primarily caused by a non-enzymatic effect triggering mitochondrial disintegration, apoptosis and cell death.
Hyperhomocysteinemia induces endothelial damage, mitochondrial disintegration, swelling of pericytes, basement membrane thickening and perivascular detachment (Weir and Molloy, 2000; Kim et al., 2002; Troen, 2005), pathologies are also seen in vaD and AD.
The exact molecular mechanisms leading to mitochondrial disintegration and neuronal apoptosis in HSD10 deficiency are still unknown but our data show that the clinical effects cannot be attributed to the accumulation of toxic metabolites in the isoleucine pathway or other metabolic effects.
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We demonstrated that mitochondrial membrane disintegration and mitochondrial dysfunction occur in the absence of any significant differences in cardiolipin amount or side chain composition in fly brains lacking iPLA2-VIA.
Proteasome inhibitors may delay CCCP-induced cell death caused by excessive Parkin activation by preventing mitochondrial membrane disintegration and cytochrome C release, whereas USP30 depletion enhances mitophagic clearance of damaged mitochondria but also has the potential to promote Parkin-induced cell death.
A prolonged period of hypoxia is then followed by a loss of mitochondrial matrix and disintegration, expansion and formation of vesicles in the endoplasmatic reticulum and cytoplasm, and lysosomal rupture with release of enzymes as a final step of cell death [6, 85].
T-cell death of type III is associated with mitochondrial swelling and disintegration.
In addition, ATP removal also prevented systemic evidence of cellular disintegration, mitochondrial damage, apoptosis, intestinal barrier disruption and even mortality.
The increased vacuolation and extensive mitochondrial swelling and disintegration seen by TEM in older hearts together with the increased levels of nitrotyrosine support the hypothesis that oxidative stress, a hallmark of ageing hearts, underlies their hypersensitivity to imatinib.
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