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Background: Nucleoside reverse transcriptase inhibitors (NRTIs) used in antiretroviral therapy may cause mitochondrial toxicity.
Oxidative mitochondrial DNA lesions and mitochondrial DNA depletion may cause mitochondrial dysfunction including in energy metabolism.
Because mitochondria are not only regulated by the nuclear genome but also by their own mtDNA, mutations within either set of DNA may cause mitochondrial disorders.
Lipotoxicity may cause mitochondrial dysfunction and subsequent liver damage and trigger inflammation [7].
It is appreciated that the increase in Bax may cause mitochondrial trans-membrane potential loss that results in the release of cytochrome c in CD4+ T cell cytosol leading to activation of caspase cascades and apoptosis [49].
GD-induced Snail (including an aggregated form) may cause mitochondrial dysfunction, facilitating ROS production in response to GD and the increased ROS may in turn enhance Snail expression to accelerate massive ROS production by RIRR and to induce GD-induced cytotoxicity and necrosis, thereby forming a positive feedback loop between Snail expression and cellular ROS levels.
Similar(45)
ACS-induced myocardial cell injury may also cause mitochondrial dysfunction.
Cisplatin may also cause mitochondrial dysfunction and increased ROS production through an impaired respiratory chain [ 118].
These data suggest that increased O2− in ECs may potentially cause mitochondrial fragmentation in the diabetic heart.
Alternatively, the decrease in OXPHOS might reflect an insufficiency of TCA carbon substrates, for the absence of autophagy-supplied substrates may also cause mitochondrial dysfunction.
The induction of mitochondrial swelling, mitochondrial membrane potential collapse, and release of cytochrome c suggests that VPA may directly cause mitochondrial damage and activate the intrinsic death-signaling pathway [ 45, 46].
More suggestions(15)
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may regulate mitochondrial
may perturb mitochondrial
may cause particular
may cause other
may be mitochondrial
may restrict mitochondrial
may indicate mitochondrial
may promote mitochondrial
may cause premature
may modify mitochondrial
may cause serious
may affect mitochondrial
may disrupt mitochondrial
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