Hydrogen sulfide: Therapeutic or injurious in ischemic stroke? Priya Gopalakrishnan, B. Shrestha, A.M. Kaskas, J. Green, J.S. Alexander, C.B. Pattillo  Pathophysiology  Volume 26, Issue 1, Pages 1-10 (March 2019) DOI: 10.1016/j.pathophys.2018.10.005 Copyright © 2018 Terms and Conditions

Fig. 1 Graphical representation depicting H2S biosynthesis and degradation. H2S biosynthesis pathways of three major cytosolic enzymes involved in endogenous H2S production: cystathionine β synthase (CBS), cystathionine γ lyase (CSE) and 3-mercaptosulfur transferase (3-MST) have been detailed in the cytosol and mitochondria. Degradation of H2S by three mitochondrial enzymes: quinone reductase (SQR), sulfur dioxygenase (SDO, ETHE1), and thiosulfate sulfurtransferase (TST) is shown within the mitochondria. Pathophysiology 2019 26, 1-10DOI: (10.1016/j.pathophys.2018.10.005) Copyright © 2018 Terms and Conditions

Fig. 2 Interactions between astrocytes and neurons for GSH and H2S handling. Astrocytes take up excess glutamate surrounding the neurons and provide a cysteine source for neuronal GSH production, both preventing neuronal excitotoxicity. Increased activity of Xc− antiporters as seen in mature neurons can heighten neuronal toxicity by H2S mediated cell death with excess glutamate by activating protease release. Pathophysiology 2019 26, 1-10DOI: (10.1016/j.pathophys.2018.10.005) Copyright © 2018 Terms and Conditions

Fig. 3 H2S-dependent signal transduction affecting stroke related events such as edema and inflammation with associated cellular events - apoptosis and gene transcription, and important stroke mediators including NfKB, Nrf2, Akt and caspase pathway. Pathophysiology 2019 26, 1-10DOI: (10.1016/j.pathophys.2018.10.005) Copyright © 2018 Terms and Conditions