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This would be in line [5], [7] one of the earliest molecular theories of ageing, which proposed that reactive oxygen species (ROS) progressively damage macromolecules, leading to a decline in cellular function and, finally, to death [11] [12].
A decline in cellular homeostasis in older individuals underlies age-related pathologies like osteoporosis and osteoarthritis.
Previous exposure to hyperglycemic conditions accelerates a decline in cellular function through metabolic memory despite normalization of glycemic control.
We hypothesized that the RyR could be either down-regulated due to a decline in cellular Ca2+ signaling or upregulated as a compensatory mechanism for the decline in IP3R protein levels and cellular signaling.
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Diabetes induced a further shift in fluorescence to the nucleus in DR-BB rats with a decline in total cellular fluorescence intensity.
The impaired insulin secretion found in T2D could be due to a decline in the cellular secretory rate (that is, in individual β-cell function), or to a decrease in β-cell mass (the product of β-cell size and number), or both.
From a physiological point of view, aging can be viewed as a continuous decline in cellular and organismal functions that (at least partially) reflects the accumulation of misfolded proteins, oxidized lipids, as well as mutated mitochondrial and nuclear DNA.
Aging causes a general decline in cellular metabolic activity, and function in different tissues and whole body homeostasis.
Gill and Holley (2004) observed that there was a rapid decline in cellular adenosine triphosphate (ATP) in Listeria monocytogenes treated with cinnamaldehyde.
This phase is characterised by a marked decline in cellular LHPs, where the decrease in Fuco levels observed after 0.5 h in HL continues, and is now also followed by a significant fall in Chl a level.
The initial activation subsided with a dramatic decline in cellular metabolism.
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CEO of Professional Science Editing for Scientists @ prosciediting.com