Molecular targets in cerebral ischemia for developing novel therapeutics.
By S. Mehta, Namratta Manhas, R. Raghubir. Brain Research Reviews, 2007
732 citations recorded by the source corpus.
Subfields: Cell Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/fcfeb7d7b9d7d170110f8ca46ce42e52cd49e996
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In Neurology
Citations in the corpus
- Mitochondria, oxidative metabolism and cell death in stroke. (2010, unknown): “However, alternative mechanisms have also been suggested to explain the protection by glutamate receptor antagonists, including interference with the propagation of potentially harmful spreading depression-like depolarizations that develop in the penumbral tissue during arterial occlusion [15,21].”
- Neuroprotection for ischemic stroke: past, present and future. (2008, background): “…et al., 2005; Trendelenburg et al., 2005) Oligendrocytes (Dewar et al., 2003) Signal transduction, general (Mattson, 1997a; Ferrer et al., 2003; Mehta et al., 2007) Intracellular signaling: kinases (Irving et al., 2002; Fukunaga et al., 2003; Perez-Pinzon et al., 2005; Zhao et al., 2006)…”
- Mitochondrial dysfunction and oxidative stress in metabolic disorders - A Step towards mitochondria based therapeutic strategies (2016, result): “In focal ischemia, the damaging action of oxidative stress in necrosis and apoptosis has been explained in previous studies [160,161].”