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Accum-ulation of oxidative stress in mitochondria is highly relevant to aging and the development of various aging-related common diseases, including cardiovascular diseases.
The oxidative modification hypothesis postulates that oxidative stress is one of the major factors in aging and the development of age-related disorders, including cardiovascular diseases.
Using mathematical models, I find that the cellular turnover rate affects the ability of genetic alterations to induce aging and the development of cancer.
If mutations occur as a result of errors during cell division, the model suggests that a low cellular turnover rate protects both against aging and the development of cancer.
Given the important signaling roles played by ROS (e.g., stimulation of mitochondrial biosynthesis, described previously), it is possible that a reduced capacity to stimulate an oxidative redox state via muscle contraction may contribute to aging and the development of chronic disease.
Little is known, however, about the degree to which normal brain aging is conserved among mammalian species, an issue of central importance in the biology of aging and the development of animal models of human neurological diseases [3].
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These results may provide a valuable foundation for understanding the molecular consequences of aging and emphasize the development of catalogues of senescence-related genes in additional tissues.
The Klotho gene plays a critical role in regulating aging and in the development of age-related diseases in mammals.
Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors both in aging and in the development of cancer.
On the opposite end of life's spectrum, recent studies using genetically-engineered mice indicate a newly recognized role for PAPP-A in aging and in the development of age-related disease.
Thus, calorie restriction slows aging and delays the development of all age-related diseases in mammals including non-human and human primates [ 13- 18].
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