<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-05-30T22:54:45Z</responseDate><request verb="GetRecord" identifier="oai:riuma.uma.es:10630/29909" metadataPrefix="marc">https://riuma.uma.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:riuma.uma.es:10630/29909</identifier><datestamp>2026-02-03T11:31:13Z</datestamp><setSpec>com_10630_2254</setSpec><setSpec>col_10630_37953</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Claros-Gil, Silvia</subfield>
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      <subfield code="a">Cabrera, Pablo</subfield>
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      <subfield code="a">Valverde, María</subfield>
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      <subfield code="a">Romero-Zerbo, Silvana Yanina</subfield>
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      <subfield code="a">López-González, Manuel Víctor</subfield>
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      <subfield code="a">Shumilov, Kirill</subfield>
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      <subfield code="a">Rivera-Ramírez, Alicia</subfield>
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      <subfield code="a">Pavía-Molina, José</subfield>
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      <subfield code="a">Martín-Montañez, Elisa</subfield>
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      <subfield code="a">García-Fernández, María Inmaculada</subfield>
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      <subfield code="c">2021-12-24</subfield>
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      <subfield code="a">Stress seems to contribute to Parkinson’s disease (PD) neuropathology, probably by dysregulation of the hypothalamic–pituitary–adrenal axis. Key factors in this pathophysiology are oxidative stress and mitochondrial dysfunction and neuronal glucocorticoid-induced toxicity. The insulin-like growth factor II (IGF-II), a pleiotropic hormone, has shown antioxidant and neuroprotective effects in some neurodegenerative disorders. Our aim was to examine the protective effect of IGF-II on a dopaminergic cellular combined model of PD and mild to moderate stress measuring oxidative stress parameters, mitochondrial and neuronal markers, and signalling pathways. IGF-II counteracts the mitochondrial-oxidative damage produced by the toxic synergistic effect of corticosterone and 1-methyl-4-phenylpyridinium, protecting dopaminergic neurons from death and neurodegeneration. IGF-II promotes PKC activation and nuclear factor (erythroid-derived 2)-like 2 antioxidant response in a glucocorticoid receptor-dependent pathway, preventing oxidative cell damage and maintaining mitochondrial function. Thus, IGF-II is a potential therapeutic tool for treatment and prevention of disease progression in PD patients suffering mild to moderate emotional stress.</subfield>
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      <subfield code="a">Claros, S.; Cabrera, P.; Valverde, N.; Romero-Zerbo, S.Y.; López-González, M.V.; Shumilov, K.; Rivera, A.; Pavia, J.; Martín-Montañez, E.; Garcia-Fernandez, M. Insulin-like Growth Factor II Prevents MPP+ and Glucocorticoid Mitochondrial-Oxidative and Neuronal Damage in Dopaminergic Neurons. Antioxidants 2022, 11, 41. https://doi.org/10.3390/antiox11010041</subfield>
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      <subfield code="a">https://hdl.handle.net/10630/29909</subfield>
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      <subfield code="a">10.3390/antiox11010041</subfield>
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      <subfield code="a">Parkinson, Enfermedad de</subfield>
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      <subfield code="a">Insulin-like Growth Factor II Prevents MPP+ and Glucocorticoid Mitochondrial-Oxidative and Neuronal Damage in Dopaminergic Neurons</subfield>
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