GIUV2016-287
La seua activitat se centra en les àrees de neurociència i investigació cardiovascular, sent els seus objectius principals l'estudi de la fisiologia de la circulació cerebral, la prevenció, fisiopatologia i tractament de l'ictus isquèmic, i la fisiopatologia de la vasculopatia diabètica, com a factor de risc cerebrovascular. Es realitza tant investigació preclínica (models animals d'ictus i diabetis) com a clínica (pacients de d'ictus).
- Fisiologia de la circulacion cerebral
- Fisiopatologia de la isquemia cerebral
- Neuroproteccion y neurorreparacion
- Diabetes y daño vascular
- Ictus isquemico agudo
- Cellular senescence as a biomaker and therapeutic target in ischaemic stroke.Brain cell senescence remains unexplored as a target for neuroprotection in stroke. The aim is to characterise brain cell senescence associated with ageing and stroke in a rat model, and to reposition a senolytic drug, Navitoclax, as an effective neuroprotectant for use as an adjunct to endovascular treatment in ischaemic stroke. The influence of gender will also be analysed.
- Analysis of thrombi obtained by mechanical thrombectomy in patients with ischemic stroke due to large vessel occlusion.In patients with large vessel ischaemic stroke, the use of thrombectomy devices makes it possible to retrieve the occluding thrombus and make it available for analysis. The thrombus can be studied fresh, frozen or fixed for preservation and subsequent analysis. The aim is to subject thrombi to different types of analysis to obtain information on their characteristics, structure and composition, and to establish associations between the nature of the thrombus and clinical-radiological variables relating to the diagnosis, treatment and prognosis of stroke. It will also help to explain the behaviour of the thrombus during fibrinolysis and/or thrombectomy, enabling research and development of more effective thrombolytic treatments and thromectomy devices.
- Mitophagy and inflammation in cerebral ischemia: therapeutic target.Inflammation and loss of mitochondrial function are involved in the development of ischemic brain damage. Mitophagy (selective degradation of damaged or dysfunctional mitochondria by autophagy) is an essential homeostatic mechanism for maintaining a healthy mitochondrial population. There is evidence to suggest that mitophagy and inflammation may be related, and thus mitophagy could be a mechanism for regulating inflammation. The objectie is to characterize brain cell mitophagy and its relationship to inflammation in a rat model of cerebral ischemia.
- Microglial polarization towards M2 phenotype as a neuroprotective mechanism after ischemic stroke.Polarisation of microglia following a cerebrovascular accident towards an M2 or anti-inflammatory phenotype could be a neuroprotective mechanism. The objective is to characterise the polarisation process of microglia and explore the use of drugs that induce this polarising effect as an option for the treatment of ischemic strokes, in both normoglycemia and hyperglycemia conditions.
Name | Nature of participation | Entity | Description |
---|---|---|---|
FRANCISCO JAVIER MIRANDA ALONSO | Director | Universitat de València | |
Research team | |||
TERESA JOVER MENGUAL | Member | Universitat de València | |
JUAN BAUTISTA SALOM SANVALERO | Member | Universitat de València | |
JOSE M CENTENO GUIL | Member | Universitat de València | |
MARIA CONSUELO BURGUETE LOPEZ | Member | Universitat de València | |
MARÍA CASTELLO RUIZ | Member | Universitat de València | |
MARIA JORQUES GONZALEZ | Collaborator | Universitat de València - Estudi General | UVEG PhD student |
MIKAHELA ANDREA LOPEZ MORALES | Collaborator | Universitat de València | |
MIKAHELA ANDREA LOPEZ MORALES | Collaborator | Universitat de València - Estudi General | UVEG PhD student |
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- Physiology
- Ischaemic stroke, cellular senescence, neuroprotection
- Ictus isquémico, trombectomía, trombo cerebroarterial
- learning outcomes, teaching innovation, professional competences
- Neurología: manejo del ictus isquémico