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It is commonly believed that aging is caused by random accumulation of molecular damage due to failure of maintenance, because repair is costly [ 1, 2].
In contrast, the molecular damage theory is about life long accumulation of random molecular damage due to failure of repair/maintenance.
If we redefine "signal transduction" as "accumulation of random molecular damage due to failure of maintenance", then yes, this is a cause of aging and age-related diseases.
Excessive reactive oxygen species (ROS) have been shown to cause cellular senescence in culture, and accumulated molecular damage due to mitochondrial ROS has long been thought to drive aging phenotypes in vivo.
Whether the ageing process itself consists of the accumulation of molecular damage due to environmental and stochastic effects or is a truly programmed or pseudo-programmed process that stems from development remains to be determined, yet a process as complex as ageing most likely involves aspects of all these phenomena [ 3- 5].
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Therefore only a set of mitochondria which are rather functional were analyzed while those which are severely impaired due to molecular damage or due to opening of the 'mitochondrial permeability transition pore' [30], [57], [58] may not band at the position where intact mitochondria are found.
To avoid molecular damage of biomolecules due to oxidation, all cells have evolved constitutive and responsive systems to mitigate and repair chemical modifications.
By the same token, "aging" due to molecular damage will not manifest itself, if aging due to hyperfunction invariably limits life span [ 122].
A fifth specimen did yield amplification products for the control and COI regions but was excluded from further analyses due to excessive molecular damage including fragmentation and type 2 miscoding lesions [13].
One of the factors known to affect thermodynamics is temperature, and therefore it has been long speculated that it may influence the ageing process with organisms ageing faster at higher temperatures due to more molecular damage being generated (Conti 2008; Liu and Walford 1972; Rikke and Johnson 2004).
Accordingly, the plant Fe deficiency response includes the induction of molecular mechanisms associated with mediation of the damage due to oxidative stress.
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