The group GE-06 “Pathophysiology of renal and vascular damage” is an Emerging Group of the IMIBIC. Our group is composed of clinical and basic researches working together to improve the knowledge of these pathologies and to translate the basic research into the clinical practice. We integrate into our studies experts in specific areas such as Immunology, Pathology, Pharmacology, Cardiology, and Nephrology to carry out several multidisciplinary research projects. The group is led by Juan Antonio Moreno, a Ramón y Cajal tenure track researcher associated with the Department of Cell Biology, Physiology and Immunology (University of Cordoba) since 2019 (103 articles published, cumulative IF: 340; H-index: 30).
Renal and cardiovascular diseases constitute major health problems, with elevated mortality and morbidity rates. Our group is unraveling novel pathogenic mechanisms involved in the development of these diseases. Our primary goal is to understand the basis for alterations in renal and vascular wall to identify new molecules involved in the progression of these pathologies that may be used as potential diagnostic/prognosis biomarkers and to develop novel therapeutic approaches and their eventual clinical translation. Specifically, we are interested in certain cellular and molecular aspects (oxidation, inflammation, apoptosis, fibrosis, transcription factors, intracellular signaling, cytokines, etc.) involved in the progression of a number of pathologies (atherothrombosis, diabetic nephropathy, glomerular diseases, acute renal injury, nephrotoxicity, renal fibrosis, among others). To achieve these objectives, our group has applied a varied set of cellular and molecular biology techniques (flow cytometry, confocal microscopy, activity assays, gene/protein expression analysis, etc) in suitable cultured cells, experimental animal models and human samples.
We have recently observed that one of the mechanisms involved in the loss of renal function is the massive accumulation of hemoglobin (Hb), myoglobin, and other heme-related proteins. Massive accumulation of hemoprotein in the kidney promotes acute kidney injury and chronic kidney disease, as observed in patients suffering from glomerular macroscopic hematuria and massive/recurrent intravascular hemolysis (atypical hemolytic uremic syndrome, paroxysmal nocturnal hemoglobinuria and sickle cell disease). A similar pathogenic role of hemoproteins has been demonstrated during the progression of hemorrhagic atherosclerotic plaques. Our group discovered new cellular targets for the adverse effects of hemoproteins (hemoglobin (Hb), myoglobin, and other heme-related proteins) in the kidney and the atherosclerotic plaque. Thus, we identified hemoproteins-mediated injury in macrophages, tubular cells, and podocytes.
We actively collaborate with numerous researchers working in national and international centers (Fundacion Jimenez Diaz, Autonoma University Madrid, Complutense University Madrid, Odense University Hospital, Denmark, Karolinska Institute, Sweden, Paris Diderot School of Medicine, France and University of Debrecen, Hungary, among others). In addition, we are an active member of the National Network on Cardiovascular Diseases (CIBERCV), Spanish Society of Atherosclerosis, Spanish Society of Nephrology (GLOSEN), and the Immunonephrology Working Group of the European Renal Association.
In the last years, we have obtained competitive research projects supported by the National Institute of Health Carlos III (ISCIII), Spanish Society of Atherosclerosis, Spanish Society of Nephrology, Iñigo Alvarez de Toledo Renal Foundation, and the IMIBIC-Roche grant, as well as different projects funded by international biotechnological companies.
CIBERCV - CIBER on Cardiovascular Diseases
ERA-EDTA - Immunonephrology Working Group. European Renal Association – European Dialysis and Transplant Association
GLOSEN - Spanish group for glomerulonephritis
- cell death
- oxidative stress
- acute kidney injury
- intravascular Hemolysis
- IgA nephropathy
Training capacity of the group
Supervised thesis in the last 5 years:
Renal damage induced by glomerular hematuria. 2016. Complutense University. Madrid.
Novel pathophysiological mechanisms involved in renal and vascular damage associated to hemoproteins accumulation. 2016. Autonoma University. Madrid.
Molecular mechanisms involved in acute kidney injury associated to rhabdomyolysis. 2018.
Value of hematuria as a risk factor in IgA Nephropathy. Complutense University. Madrid. 2020.
Human resources obtained in national or international calls in the last 5 years:
Conchita Rábago Fellowship, Fundación Conchita Rábago, 2016-2018.
FPU16/03600. MICINN, 2017-2021
PFIS FI18/00310. Instituto de Salud Carlos III, 2019-2022
Cordoba University PhD Fellowship, 2020-2022
Sara Borrell CD17/00030. Instituto de Salud Carlos III, 2018-2019
Sara Borrell CD19/00021. Instituto de Salud Carlos III, 2020-2022
Participation in international R&D&I projects in the last 5 years:
Effect of Budesonide Treatment on Hb-associated renal biomarkers in patients with IgA nephropathy. Pharmalink AB, Sweden. 2017-2020.
COST Action CA18216 - Network for Research in Vascular Ageing. European Cooperation in Science and Technology. Horizon 2020 Framework Programme of the European Union. 2019-2023.
FP7-HEALTH-2013.4.1-4-602422. KidneyConnect: European Kidney-Podocyte Research Platform. 2013-2016.
Immnunonephrology working group (IWG). The European Renal Association – European Dialysis and Transplant Association (ERA-EDTA). 2018-2020
To identify new pathological effects and novel molecular pathways involved in vascular and renal damage.
To validate the effectiveness of novel therapeutic strategies in these pathological conditions.
To analyze the prognostic value of different biomarkers differently expressed in biopsies, blood, and urine samples from patients with renal and vascular diseases.