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Determine pathways by which chronic inflammation damages macromolecules or disrupts tissue homeostasis in the context of age-related disease.
Given the current hypothesis that cancer arises from cancer stem cells (CSCs), the mechanism by which chronic inflammation leads to the emergence of CSCs needs to be addressed.
Four sessions explored the intrinsic, environmental exposures and immune pathways by which chronic inflammation are generated, sustained, and lead to age-associated diseases.
It is clear that, for multiple types of infections, aberrant DNA methylation is induced via chronic inflammation, but the molecular mechanisms by which chronic inflammation induces aberrant DNA methylation are mostly still unclear.
A possible role is suggested for IL-6, which reduces insulin-like growth factor 1 production, providing a major mechanism by which chronic inflammation inhibits hormonal anabolic action and affects growth [ 43].
Even though the mechanisms by which chronic inflammation leads to carcinogenesis are not fully understood, it is generally accepted that inflammation results in repeated DNA damage and in the accumulation of genetic defects (McKay et al, 2008).
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RA is characterised by a symmetrical polyarthritis in which chronic inflammation of joints is associated with a progressive destruction of cartilage and bone, leading to functional decline and disability.
Examples include allergic, or hypersensitivity, reactions, in which an environmental agent such as pollen, which normally poses no threat to the individual, stimulates inflammation, and autoimmune reactions, in which chronic inflammation is triggered by the body's immune response against its own tissues.
The precise mechanism by which chronic colonic mucosal inflammation causes malignancy in this context is poorly understood, although it is supposed to be related to a failure in regulatory mechanisms during cell division.
However, the mechanisms by which chronic cigarette smoking causes the lung inflammation and damages leading to COPD have not been clarified.
Our findings, along with the literature reviewed below, suggest that chronic inflammation and oxidation may be mechanisms by which chronic depression can result in shortened telomeres.
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