A5036159024- Cardiovascular Function and Risk Factors
- Parathyroid Disorders and Treatments
- Renin-Angiotensin System Studies
- Galectins and Cancer Biology
- Hormonal Regulation and Hypertension
- Diabetes Treatment and Management
- Metabolism, Diabetes, and Cancer
- Vitamin D Research Studies
- Heart Failure Treatment and Management
- COVID-19 Clinical Research Studies
- Peptidase Inhibition and Analysis
- Adipose Tissue and Metabolism
- Lipoproteins and Cardiovascular Health
- Atrial Fibrillation Management and Outcomes
- Adipokines, Inflammation, and Metabolic Diseases
- Cellular transport and secretion
- Gut microbiota and health
- Ubiquitin and proteasome pathways
- Acute Myocardial Infarction Research
- Cardiac Health and Mental Health
- Diet and metabolism studies
- GDF15 and Related Biomarkers
- Atherosclerosis and Cardiovascular Diseases
- Liver Disease Diagnosis and Treatment
- Magnesium in Health and Disease
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas
2015-2025
Hospital Universitario Fundación Jiménez Díaz
2015-2024
Universidad Autónoma de Madrid
2014-2024
Centre for Biomedical Network Research on Rare Diseases
2024
Instituto de Salud Carlos III
2021-2024
Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition
2021-2022
Universidad de Salamanca
2019
Hospital Universitario de Móstoles
2017
Hospital Universitario de Fuenlabrada
2017
Hospital Universitario Fundación Alcorcón
2017
Abstract Early since the onset of COVID-19 pandemic, medical and scientific community were aware extra respiratory actions SARS-CoV-2 infection. Endothelitis, hypercoagulation, hypofibrinolysis identified in patients as subsequent responses endothelial dysfunction. Activation barrier may increase severity disease contribute to long-COVID syndrome post-COVID sequelae. Besides, it cause alterations primary, secondary, tertiary hemostasis. Importantly, these have been highly decisive evolution...
Abstract Background Hyperinflammation, hypercoagulation and endothelial injury are major findings in acute post-COVID-19. The SARS-CoV-2 S protein has been detected as an isolated element human tissues reservoirs is the main product of mRNA COVID-19 vaccines. We investigated whether alone triggers pro-inflammatory pro-coagulant responses primary cultures two cell types deeply affected by SARS-CoV-2, such monocytes cells. Methods In umbilical vein cells (HUVEC) monocytes, components NF-κB...
Abstract —Nuclear factor-κB (NF-κB) regulates many genes involved in vascular physiopathology. We have previously observed vivo NF-κB activation injured vessels that diminished by angiotensin-converting enzyme inhibition. In the present work, we investigated effect of angiotensin II (Ang II) on activity rat smooth muscle cells, evaluating molecular mechanisms and specific receptor subtype involved. Ang increased DNA binding (5-fold, 10 − 9 mol/L at 1 hour; electrophoretic mobility shift...
Background— Angiotensin II (Ang II) participates in the development of fibrosis during vascular damage. Connective tissue growth factor (CTGF) is a novel fibrotic mediator. However, potential link between CTGF and Ang has not been investigated. Methods Results— In vivo effects were studied by systemic infusion into normal rats to evaluate extracellular matrix protein (ECM) expression immunohistochemistry. aorta II–infused rats, staining was markedly increased ECM overexpression observed. An...
Abstract Angiotensin-converting enzyme (ACE) inhibitors reduce macrophage infiltration in several models of renal injury. We approached the hypothesis that angiotensin II (AngII) could be involved inflammatory cell recruitment during damage through synthesis monocyte chemoattractant protein-1 (MCP-1). In a model immune complex nephritis, we observed an up-regulation MCP-1 (mRNA and protein) coincidentally with mononuclear were markedly reduced by treatment ACE inhibitor quinapril. Exposure...
Inflammatory cell infiltration plays a key role in the onset and progression of renal injury. The NF-κB participates inflammatory response, regulating many proinflammatory genes. Angiotensin II (Ang II), via AT1 AT2 receptors, activates NF-κB. Although contribution Ang to kidney damage is already established, receptor subtype involved recruitment not clear. For investigating this issue, unilateral ureteral obstruction (UUO) model was used mice, blocking production/receptors pathway. Two days...
Visfatin/extracellular-nicotinamide-phosphoribosyltranferase-(eNampt) is a multifaceted adipokine enhanced in type-2-diabetes and obesity. Visfatin/eNampt cause vitro endothelial dysfunction vascular inflammation, although whether the same effects are achieved vivo unknown. Toll-like receptor-4 (TLR4), main surface pattern recognition receptor of innate immune system potential target for visfatin/eNampt. We studied its capacity to generate vivo, focusing on TLR4 role downstream activation...
Background and Aims: Recent studies suggest that mitochondrial dysfunction promotes progression to NASH by aggravating the gut‐liver status. However, underlying mechanism remains unclear. Herein, we hypothesized enhanced activity might reshape a specific microbiota signature that, when transferred germ‐free (GF) mice, could delay progression. Approach Results: Wild‐type methylation‐controlled J protein knockout (MCJ‐KO) mice were fed for 6 weeks with either control or choline‐deficient,...
The aim of this paper is to study the myocardial damage secondary long-term streptozotocin-induced type 1 diabetes mellitus (DM1). Normotensive and spontaneously hypertensive rats (SHR) received either streptozotocin injections or vehicle. After 22 6 wk, DM1, SHR, DM1/SHR, control were killed, left ventricles studied by histology, quantitative PCR, Western blot, ELISA, electromobility shift assay. Cardiomyocyte cultures also performed. expression profibrotic factors, transforming growth...
BackgroundMyocardial fibrosis is a key process in diabetic cardiomyopathy. However, their underlying mechanisms have not been elucidated, leading to lack of therapy. The glucagon-like peptide-1 (GLP-1) enhancer, sitagliptin, reduces hyperglycemia but may also trigger direct effects on the heart. MethodsGoto-Kakizaki (GK) rats developed type-II diabetes and received an anti-hyperglycemic drug (metformin) or vehicle (n=10, each). After cardiac structure function assessment, plasma left...