Khoshnam, S.E., Winlow, W., Farzaneh, M., Farbood, Y. and Moghaddam, H.F. (2017) Pathogenic Mechanisms Following Ischemic Stroke. Neurological Sciences, 38, 1167-1186.
https://doi.org/10.1007/s10072-017-2938-1

has been cited by the following article:

• TITLE: Pathophysiology of Cerebral Ischemia: Role of Oxidative/Nitrosative Stress

  AUTHORS: Hiba A. Awooda

  KEYWORDS: Reactive Oxygen Species, Reactive Nitrogen Species, Cerebral Ischemia, Oxidative Stress

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.7 No.3, March 6, 2019

  ABSTRACT: Stroke is a devastating disease with a complex pathophysiology; it ranks second to ischemic heart disease as a cause of death and long-term disability. Tissue damage results from diverse mechanisms with central involvement of free radicals’ overproduction that results in oxidative stress and hence contributes to brain damage. Free radicals [Reactive oxygen species/Reactive nitrogen species] play central a role in the diverse normal physiological processes and as defense mechanisms against harmful substances. When the rate of their production exceeds the anti-oxidant capacity of the body, oxidative stress occurs. Oxidative stress is implicated in the pathogenesis of various diseases including hypertension, atherosclerosis, diabetes mellitus and cancer; they mediate damage to cell structures, lipid peroxidation, protein denaturation, nucleic acid and DNA damage.