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Joaquín Jordán

Researcher at University of Castilla–La Mancha

Publications -  155
Citations -  14104

Joaquín Jordán is an academic researcher from University of Castilla–La Mancha. The author has contributed to research in topics: Mitochondrion & Programmed cell death. The author has an hindex of 45, co-authored 154 publications receiving 12336 citations. Previous affiliations of Joaquín Jordán include University of Chicago & Universidad Miguel Hernández de Elche.

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Veratridine induces apoptotic death in bovine chromaffin cells through superoxide production.

TL;DR: The results indicate that chromaffin cells share with neurons the molecular machinery involved in apoptotic death and might be considered a good model to study neuronal death during neurodegeneration.
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Role and regulation of p53 in depolarization-induced neuronal death.

TL;DR: The results suggest that p53-expression is involved in veratridine-induced neuronal death and that p 53 might be a link between toxic stimuli of different types and neuronal death.
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Phosphodiesterase 5 inhibitors prevent 3,4‐methylenedioxymethamphetamine‐induced 5‐HT deficits in the rat

TL;DR: Sildenafil protects against MDMA‐induced long‐term reduction of indoles by a mechanism involving increased production of cGMP and subsequent activation of PKG and mitochondrial ATP‐sensitive K+ channel opening.
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Superoxide anions mediate veratridine-induced cytochrome c release and caspase activity in bovine chromaffin cells

TL;DR: In conclusion, superoxide anions seem to mediate veratridine‐induced cytochrome c release, decrease in total glutathione, caspase activation and cell death in bovine chromaffin cells.
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Pyruvate protects cerebellar granular cells from 6-hydroxydopamine-induced cytotoxicity by activating the Akt signaling pathway and increasing glutathione peroxidase expression.

TL;DR: It is suggested that pyruvate, besides the anti-oxidant properties related to its structure, exerts cytoprotective actions by activating different anti-apoptotic routes that include gene regulation and Akt pathway activation.