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Altogether these findings support the view that nonischemic mechanisms are implicated in the pathophysiology of TBI.
Cytokines are implicated in the pathophysiology of major depressive disorder (MDD).
Decreased CSE and HO-1, as well as diminished H2S and reduced NO, are implicated in the pathophysiology of atherosclerosis [2, 13, 57 60].
There is increasing evidence that abnormal cytokine expression and increased metalloproteinase activity are implicated in the pathophysiology of acute coronary syndromes.
Hyperinsulinemia and insulin resistance are implicated in the pathophysiology of polycystic ovary syndrome, a condition associated with elevated levels of LH.
Therefore, increased nitrotyrosine formation may be associated with reduced bioavailability of NO [40], and both elevated nitrotyrosine as well as low levels of NO are implicated in the pathophysiology of atherosclerosis [41, 42].
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The result provides evidence that the glutamatergic system is implicated in the pathophysiology of migraine.
Reactive oxygen species (ROS) have been implicated in the pathophysiology of the brain after ischemic stroke.
Conversely, iron deficiency has been implicated in the pathophysiology of RLS [11].
Sex steroids also may have been implicated in the pathophysiology of TTH.
The adipocyte hormone leptin has been implicated in the pathophysiology of preeclampsia and in enhancing immunity.
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