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ROMs are highly unstable in nature, but their presence for short duration in the cells may lead cellular damages [19], [20].
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In conclusion, prolonged exposure to hypoxia may lead to cellular dysfunction beyond that directly involving the production of adipokines, such as in disruption to cellular glucose and lipid metabolism; this may underscore the initiation and progression of obesity-related disorders.
Premature stimulation of cellular metabolism before mitochondria have regained their ability to respond adequately in terms of energy production may lead to cellular compromise.
This 'Fenton reaction' may lead to cellular changes (e.g., DNA damage (a pro-carcinogenic effect)) and lung inflammation (Hardy and Aust 1995; Kane 1996).
Impaired elastic energy storage by extracellular matrices may lead to cellular damage and changes in signaling by mechanochemical transduction at the extracellular matrix cell interface.
Taken together, studies in patients and in Scn5a+/− mice strongly suggest that a primary abnormality in Nav1.5 channel may lead to cellular damage.
However, the release of cathepsin in excess may lead to cellular necrosis (Paquet et al, 2005).
Both the mTORC1-mediated growth stimulation and p53/p21-mediated p53/p21-mediatedt may lead to cellular senescycle (Demidenko & Blarrestonny, 2008).
ARID1A mutation may lead to cellular dysfunction as aberrant chromatin remodelling and alterations in the cell cycle checkpoints [ 98].
Unscheduled activation of the MAPK pathway may lead to cellular senescence, which could function to limit tumour development (Courtois-Cox et al, 2006).
Excess ROS may lead to cellular damage, which has been implicated in with the development of insulin resistance [ 73], and apoptosis of myoblasts [ 74].
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