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For instance, a cell undergoing protein stress may actively decrease mitochondrial function in order to 'silence' the major source of ROS, since increased ROS levels combined with proteotoxic stress would have a devastating effect on cellular functioning18.
However, A2E has also been suggested to directly decrease mitochondrial function and disrupt cellular homeostasis by several mechanisms.
The data suggest that supraphysiological doses of pyruvate decrease mitochondrial function despite limited biogenesis and that anaplerotic agents can reverse this effect.
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In addition, telomere dysfunction decreases mitochondrial function by affecting downstream gene expression of cell energy regulators such as p53 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α).
A previous report suggests that human epidermal cells exposed to ZnO NPs reflect abnormal morphology, cellular shrinkage, detachment from the surface of the flask as well as decreased mitochondrial function, and significantly increased LDH[15, 16] at concentrations of 5 to 20 μg mL−1 after 24-h exposure[6].
In vitro cell line studies have shown decreased mitochondrial function and oxidative stress after exposure to ZnO NPs in human embryonic lung fibroblasts (HELF) cells[7], human epidermal (A431) cells[8], human colon carcinoma (LoVo) cells[9], human lung bronchial epithelial (BEAS-2B) cells[10], hepatocellular carcinoma SMMC-77211) cells[11], and human osteoblast cancer cell line[12].
We observed decreased mitochondrial function in patients on high dose simvastatin treatment, with no signs of myopathy [10].
Following Warburg's observations, this mutation causes decreased mitochondrial function, compensatory increase in glycolysis and accelerated growth in vivo.
Our present observations of increased superoxide generation and decreased mitochondrial function modified by rotenone in STAT3-CKO cells support this novel mechanism of STAT3 action in cortical astrocytes.
To establish whether the decreased mitochondrial function in muscle of septic patients is due to a decreased synthesis of mitochondrial proteins, in vivo protein synthesis rates of mitochondrial protein was determined.
Because oxygen is the main substrate of the ETC, hypoxic conditions consequently decreases mitochondrial function and initiates expression of a host of genes that are needed for compensatory ATP production by glycolysis.
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