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At 5 days post-infection (Fig. 3A), we observed several significant changes in gene expression that may impact mitochondrial polarization.
Accordingly, FM may impact mitochondrial oxidation to meet the increased metabolic demand during exercise, which would lead to a lower rOEF as observed in the present study.
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Also, ionic currents may directly impact mitochondrial function itself, as it has been previously demonstrated that high Ca2+ inhibits mitochondrial respiration, dissipates membrane potential, and suppresses ATP production [ 26, 27].
Therefore, tools capable of minimizing mitochondrial Ca2+ overload would decrease mitochondrial ROS accumulation and improve mitochondrial energy production, which may impact on mitochondrial-oxidative mediated diseases.
This is the first experimental evidence that uncoupling in vivo can impact mitochondrial number and function.
Such unusual structures may influence the efficiency of mtDNA replication and transcription (Brown et al. 1986; Pereira et al. 2008) and thus regulate mtDNA content in cells, which may impact the efficiency of mitochondrial function (Suissa et al. 2009), and contribute to adaptation (Cheng et al. 2013).
The differences in mitochondrial number may impact their capacity to match critical functions to ATP generation with metabolic consequences.
Changes in mitochondrial function may impact protein metabolism since protein synthesis and ubiquitin-dependent protein degradation are ATP-dependent.
Severe mitochondrial alterations that may impact the energy status are also found in these cells.
The extensive protein-protein interactions occurring in the inner mitochondrial membrane translocase complex suggest that variation in FXC1 protein sequence caused by polymorphisms in its poly-Q region may have potential for impacting mitochondrial function [ 55].
In trying to understand the reasons for these differences, it is worth noting that the seemingly straightforward functional subclassification of PINK1 and Parkin mutations as principally affecting mitochondrial quality control, and Mfn2 and Opa1 mutations as primarily impacting mitochondrial dynamism, may be misleading.
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