{"id":14,"date":"2022-07-20T11:50:39","date_gmt":"2022-07-20T11:50:39","guid":{"rendered":"https:\/\/blogdev.uclm.es\/fullsite\/?page_id=14"},"modified":"2026-02-13T10:23:23","modified_gmt":"2026-02-13T10:23:23","slug":"investigacion","status":"publish","type":"page","link":"https:\/\/blog.uclm.es\/Geon\/investigacion\/","title":{"rendered":"Research lines"},"content":{"rendered":"\n
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\u2022 Modulation\u00a0of\u00a0oxidative stress in\u00a0glioblastoma and\u00a0its\u00a0metabolic reprogramming<\/p>\n\n\n\n

Glioblastoma is\u00a0the\u00a0most\u00a0frequent\u00a0CNS tumor\u00a0withthe\u00a0worst\u00a0prognosis.\u00a0We\u00a0are\u00a0studying\u00a0in in vitro and in vivo models\u00a0how pretreatment\u00a0with\u00a0coenzyme\u00a0Q10\u00a0remodels\u00a0the\u00a0tumor\u00a0metabolism\u00a0and\u00a0proteome,\u00a0preventing\u00a0aerobic\u00a0glycolysis\u00a0
(Warburg\u00a0effect),\u00a0which\u00a0has\u00a0an\u00a0immediate\u00a0impact on\u00a0tumor\u00a0growth\u00a0and\u00a0invasion\u00a0producing\u00a0a\u00a0decrease\u00a0in glioblastoma\u00a0cell\u00a0
viability in vitro and\u00a0triplicates\u00a0the\u00a0effect\u00a0of\u00a0short and\u00a0long\u00a0term\u00a0radiotherapy\u00a0and\u00a0the proapoptotic\u00a0effect\u00a0of\u00a0
temozolomide.<\/p>\n\n\n\n

<\/p>\n\n\n\n

<\/p>\n\n\n\n

\u2022 Neuroprotective role of coenzyme Q10 in proteostasis during Alzheimer’s disease (AD) <\/p>\n\n\n\n

A common aspect of neurodegenerative diseases is the increasedproduction of reactive oxygen species (ROS) 
due to mitochondrial dysfunction. The increase in ROS alters cellular proteostasis by the imbalance between 
the response to misfolded proteins (UPR), proteasomal protein degradation (ERAD) and autophagy, leading to 
cell vulnerability and cell death by apoptosis. We are studying the interrelationship between oxidative
stress and proteostasis, establishing their spatiotemporal dynamics, in in vitro and in vivo models and the
early regulation of the level of oxidative stress with ubiquinol supplementation in prodromal and premorbid 
stages of the disease, to control cellular proteostasisand thus slow the progression of AD-associated 
pathophysiology in the 3xTg-AD murine model of this disease. We have also evaluated the impact of ubiquinol 
on cerebral vascular endothelial compromise in AD. Vascular dysfunction maycontribute to the development 
and progression of AD according to epidemiological and experimental data. There are numerous structural and 
functional abnormalities of the microvasculature in these patients. The \u00df-amyloid peptide damages the 
endothelium inducing the generation of ROS mediated by the activation of NADPH oxidase and by its incorporation
into the mitochondria causing mitochondrial dysfunction.<\/p>\n\n\n\n

<\/p>\n\n\n\n

<\/p>\n\n\n\n

\u2022 Early diagnosis of AD<\/p>\n\n\n\n

In\u00a0the\u00a0last\u00a0years,\u00a0we\u00a0are\u00a0setting\u00a0up\u00a0different\u00a0approachesoriented\u00a0to\u00a0an\u00a0early\u00a0diagonosis\u00a0of\u00a0AD,\u00a0based\u00a0on\u00a0accelerated cell aging and transdifferentiation\u00a0into\u00a0neurons (ongoing).<\/p>\n\n\n\n

<\/p>\n\n\n\n

<\/p>\n\n\n\n

\u2022 Safety of graphene and related materials<\/p>\n\n\n\n

We have been collaborating with the MSOC group<\/a> of the University of Castilla-La Mancha, testing the toxicity and genotoxicity of a family of graphene-related materials and other 2D materials. Moreover, recently, we have adapted and standardized OECD methods to properly test the effects of these compounds on human epidermal cells.<\/p>\n<\/div>\n<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

\u2022 Modulation\u00a0of\u00a0oxidative stress in\u00a0glioblastoma and\u00a0its\u00a0metabolic reprogramming Glioblastoma is\u00a0the\u00a0most\u00a0frequent\u00a0CNS tumor\u00a0withthe\u00a0worst\u00a0prognosis.\u00a0We\u00a0are\u00a0studying\u00a0in in vitro and in vivo models\u00a0how pretreatment\u00a0with\u00a0coenzyme\u00a0Q10\u00a0remodels\u00a0the\u00a0tumor\u00a0metabolism\u00a0and\u00a0proteome,\u00a0preventing\u00a0aerobic\u00a0glycolysis\u00a0(Warburg\u00a0effect),\u00a0which\u00a0has\u00a0an\u00a0immediate\u00a0impact on\u00a0tumor\u00a0growth\u00a0and\u00a0invasion\u00a0producing\u00a0a\u00a0decrease\u00a0in glioblastoma\u00a0cell\u00a0viability in vitro and\u00a0triplicates\u00a0the\u00a0effect\u00a0of\u00a0short and\u00a0long\u00a0term\u00a0radiotherapy\u00a0and\u00a0the proapoptotic\u00a0effect\u00a0of\u00a0temozolomide. \u2022 Neuroprotective role of coenzyme Q10 in proteostasis during Alzheimer’s disease (AD)  A common aspect of neurodegenerative diseases is the increasedproduction of reactive oxygen species (ROS) due to mitochondrial dysfunction. The increase in ROS alters cellular proteostasis by the imbalance between the response to misfolded proteins (UPR), proteasomal protein degradation (ERAD) and autophagy, leading to cell vulnerability and cell death by apoptosis. We are studying the interrelationship between oxidativestress and proteostasis, establishing their spatiotemporal dynamics, in in vitro and in vivo models and theearly regulation of the level of oxidative stress with ubiquinol supplementation in prodromal and premorbid stages of the disease, to control cellular proteostasisand thus slow the progression of AD-associated pathophysiology in the 3xTg-AD murine model of this disease. We have also evaluated the impact of ubiquinol on cerebral vascular endothelial compromise in AD. Vascular dysfunction maycontribute to the development and progression of AD according to epidemiological and experimental data. There are numerous structural and functional abnormalities of the microvasculature in these patients. The \u00df-amyloid peptide damages the endothelium inducing the generation of ROS mediated by the activation of NADPH oxidase and by its incorporationinto the mitochondria causing mitochondrial dysfunction. \u2022 Early diagnosis of AD In\u00a0the\u00a0last\u00a0years,\u00a0we\u00a0are\u00a0setting\u00a0up\u00a0different\u00a0approachesoriented\u00a0to\u00a0an\u00a0early\u00a0diagonosis\u00a0of\u00a0AD,\u00a0based\u00a0on\u00a0accelerated cell […]<\/p>\n","protected":false},"author":376,"featured_media":0,"parent":0,"menu_order":2,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-14","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/pages\/14","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/users\/376"}],"replies":[{"embeddable":true,"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/comments?post=14"}],"version-history":[{"count":25,"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/pages\/14\/revisions"}],"predecessor-version":[{"id":768,"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/pages\/14\/revisions\/768"}],"wp:attachment":[{"href":"https:\/\/blog.uclm.es\/Geon\/wp-json\/wp\/v2\/media?parent=14"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}