Fisiopatologia Renal

El nostre principal interès científic és entendre, des d’una aproximació multidisciplinària i translacional, els processos moleculars i cel·lulars que duen a una disfunció renal en diferents patologies del ronyó. Concretament, les nostres principals línies de recerca són les següents:

Estudi de la fisiopatologia de les tubulopaties renals rares hereditàries.
Comprensió dels mecanismes de dany i regeneració renal.
Estudi del desenvolupament del carcinoma renal de cèl·lules clares (CCRCC, per les seves sigles en anglès).
Estudi de l’impacte dels andrògens en aquests processos.

Som experts en el següent:

Generació de models cel·lulars de patologies renals amb alteracions genètiques específiques.
Models animals modificats genèticament i amb teràpia gènica
Tècniques de microscòpia d’alta resolució en temps real
Treball amb mostres de pacients per a fer recerca translacional.

En conjunt, la nostra investigació té com a objectiu combinar dades «òmiques» de models cel·lulars i animals amb dades de pacients per a desenvolupar nous biomarcadors i possibles tractaments de diverses patologies renals.

Línies de recerca

Recerca Clínica i Translacional en Demència

The primary objective of this research line is to deepen the understanding of the pathophysiology of cerebral amyloid angiopathy (CAA), a neurovascular disease linked to Alzheimer’s and other cognitive disorders. More specifically, the focus is on identifying diagnostic and clinical progression biomarkers in patients with intracerebral hemorrhage and CAA, as well as investigating new therapeutic strategies in models of cerebral beta-amyloidosis, with the goal of improving the treatments available for these conditions.

IP: Maria Pilar Delgado Martínez

Recerca Clínica i Translacional en Demència

IP: Maria Pilar Delgado Martínez

Androgen activity in renal pathophysiology: Identification of androgen-regulated kidney-specific genes and functional characterization of them, in processes of inflammation, oxidative stress and fibrosis underlying chronic kidney disease, hypertension and metabolic syndrome.

Among the genes identified in our laboratory that are kidney-specific and regulated by androgens at the transcriptional level we are particularly focused on the one that codes for the kidney androgen-regulated protein (KAP). Besides characterization of the functional promoter elements that enable KAP expression in proximal tubule epithelial cells, we have generated a transgenic (Tg) mouse model that overexpresses KAP in proximal tubule cells under the presence of androgens, in order to mimick the endogenous KAP expression pattern. KAP Tg mice show altered lipid metabolism, glycosuria, proteinuria and hypertension, as well as focal segmental glomerulosclerosis mediated by increased oxidative stress. We are currently working in this Tg model and also preparing conditional knock-out mice to further caharacterize the role of KAP in renal pathophysiology. Moreover, we are also studying the role of KAP in the metabolic syndrome. Besides KAP, we are studying the role of KAP-interacting immunophilins in inflammation and kidney fibrosis.

IP: Androgen activity in renal pathophysiology: Identification of androgen-regulated kidney-specific genes and functional characteri

Focal segmental glomerulosclerosis

Idiopathic nonfamilial focal segmental glomerulosclerosis (FSG) is a disease with no treatment, whose usual outcome is end-stage renal disease frequently recidivating after transplantation. In close cooperation with the Nephrology and Paediatric Nephrology services of Vall d'Hebron hospital together with hospitals throughout the country that provide a significant number of patients, we intend to identify the hypothetical blood factor that causes the proteinuria observed in this disease. Identification of such plasma factor, by means of differential proteomic analysis, would allow the definition of therapeutic targets for the disease, which currently lacks an effective treatment. Our second objective is to find biomarkers that enable us to foresee a potential recidivation and the consequent loss of the graft following renal transplantation to FSG patients.

IP: Joan López Hellin