Luis B. Tovar y Romo

Luis B. Tovar y Romo

Neuropatología Molecular

ltovar@ifc.unam.mx

AL-305

Tel. +52 55 56225731

Intereses de Investigación

Our research focuses on the cellular and molecular mechanisms that are activated upon brain and spinal cord damage and the processes involved in neuronal recovery after injury. We are especially interested in understanding endogenous processes that promote functional recovery after stroke.


Trayectoria profesional

Investigador Titular A, SNI I

Instituto de Fisiología Celular (desde 2013)

Universidad Nacional Autónoma de México


Posdoctorados y estancias

Translational Gerontology Branch (2018, 2019)

National Institute on Aging / National Institues of Health, Baltimore MD, USA


Departamento de Neurología (2010-2013)

Johns Hopkins University School of Medicine, Baltimore, EEUU


Institut de Biologie du Développement (2008)

IBDML - Institut National de la Santé et de la Recherche Médicale, Marsella - Francia


Formación académica

Doctorado en Ciencias Biomédicas - Neurociencias (2005-2009)

Instituto de Fisiología Celular - UNAM, México


Licenciatura en Investigación Biomédica Básica (1999-2004)

Instituto de Fisiología Celular - UNAM, México


Premios y distinciones

  • Medalla Alfonso Caso, Doctorado en Ciencias Biomédicas, Universidad Nacional Autónoma de México. (2009)
  • Premio "Dr. Maximiliano Ruiz Castañeda". Academia Nacional de Medicina de México. (2011)
  • IBRO Return Home Program Award. International Brain Research Organization. (2014)
  • Estímulo a Investigaciones Médicas - Fundación Miguel Alemán (2015)

Líneas de Investigación

Structural remodeling and functional recovery in response to neuronal damage : Cerebral ischemic stroke, caused by the obstruction of blood flow, causes a very rapid neuronal death in the lesion core and activates chronic neurodegenerative processes in the area of penumbra. A series of endogenous processes are activated in response to neurodegeneration, among them are the formation of new blood vessels in a process called angiogenesis and the proliferation of neuronal progenitors in a process known as neurogenesis. Both these processes are presumably involved in the functional recovery that occurs immediately after ischemia. In this research we aim to understand the molecular mechanisms activated by the ischemic process that intervene in the structural remodeling of the affected brain and in the maintenance of neuronal function. We mimic the molecular events induced by hypoxia in vascular and neuronal progenitor cultures, and analyze their effects on the activation of intracellular responses that promote neuronal survival. We integrate all histological, physiological and behavioral responses driven by signaling pathways with the use of in vivo stroke models.

Proteomic profiling of exosomes derived from brain cells under hypoxia : Extensive data analyses of protein content have been recently conducted in many different populations of extracellular vesicles. Exosomes, formed in late endosomes and released to the extracellular milieu conveying chemical messages to distant targets, have uncovered complex systems of distant cell-to-cell communication. All cell types synthesize and release exosomes upon stress activation, and the characterization of their proteomic content might enable the identification of target signaling that would unveil systemic adaptive responses to stress. Under this premise, we study the protein content of brain microvascular endothelial cells (BMEC), astrocytes and neural precursor-derived exosomes following hypoxia.

Axonal regeneration following stroke : In the pathophysiology of ischemic stroke, a phase of spontaneous recovery has been described. This is mediated through different mechanisms, one of which could involve processes of axonal regeneration. This process could also be promoted by cellular factors released by astrocytes, for example, those contained in exosomes that have an important neuroprotective effect. We investigate whether the administration of exosomes derived from astrocytes promotes reinnervation and/or axonal regeneration after cerebral ischemia in an experimental model of ischemic cerebral infarction.


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