Head of the Research Group on “Biomarkers for Cardiovascular Disease Evolution” at the Reseach Institut of the Hospital Santa i Sant Pau (FIR-HSCSP) in Barcelona, Spain. She has been initially training and after staff member in prominent Institutions in Europe, the Gaubius-Institute TNO in Leiden (The Netherlands, 3 years) with an EU postdoctoral contract, and the Faculty of Medicine in Westfälische Wilhelms-Universität Münster (Germany, 12 years), initially with a postdoctoral contract from the Alexander von Humboldt Foundation and later in the framework of contracts with the University of Münster and the prestigious German Research Foundation DFG (Deutsche Forschungsgemeinschaft).
EDUCATION
PhD in Biology
RESEARCH INTERESTS
Biomarkers (e.g proteins, coding and non-coding RNAs) in Cardiovascular and coronary ischemic disease; atherosclerosis, vascular and myocardial remodeling, atherothrombosis
miRNA Expression Profile in Whole Blood of Healthy Volunteers and Moderate Beer Consumption with Meals Teresa Padro, Rafael Escate, Lina Badimon Nutrients, 2026 Background/Objectives: Moderate consumption of fermented beverages such as traditional beer has been associated with antioxidant and anti-inflammatory effects. MicroRNAs (miRNAs) play key roles in inflammation and oxidative stress, yet the impact of moderate fermented beverage consumption on blood miRNA profiles remains poorly understood. This study investigated the effects of regular, moderate intake of traditional and alcohol-free beer on whole blood miRNA levels in healthy adults. Methods: Whole blood samples were collected at baseline and after a 4-week intervention with alcohol-free beer and traditional beer in healthy overweight/obese adults (n = 36). miRNA profiling was performed using Affymetrix in a discovery subset, followed by targeted validation using real-time PCR in the full cohort. Bioinformatics and system biology analysis were applied to explore potential functional associations. Results: After traditional beer consumption, 202 miRNAs showed differential expression compared to baseline (p < 0.05). Eighteen miRNAs with changes ≥1.5-fold and the two miRNAs with the lowest p-values (p < 0.005) were selected for further analysis. Of them, the six miRNAs with the most consistent expression patterns were validated by real-time PCR. Moderate beer intake was associated with increased levels of miR-144-5p and miR-19a-3p in the overall population. Sex-stratified analyses suggested a tendency toward higher levels in these miRNAs in women following traditional beer intake. In silico analysis showed that predicted target genes of these miRNAs are involved in pathways related to immune regulation and inflammatory signaling. Conclusions: Moderate beer consumption is associated with consistent changes in whole-blood miRNA expression, particularly miR-144-5p and miR-19a-3p, in a healthy overweight/obese population. These findings support a potential role for epigenetic modulation in the biological response to moderate beer intake and provide a basis for future mechanistic studies.
Lipoprotein-Specific Fatty Acid Profiles in Familial Hypercholesterolemia: Associations with Cardiovascular History and Dietary Patterns Anallely López-Yerena, Raquel Arroyo-Olivares, Victoria Santisteban, Natalia Muñoz-Garcia, Ramón Estruch, et al. Nutrients, 2026 Background/Objectives: Familial hypercholesterolemia (FH) is an autosomal dominant inherited disease characterised by lifelong LDL cholesterol levels and premature presentation of cardiovascular disease if left untreated. Whether fatty acid (FA) composition in lipoproteins is modified in FH patients is not known. This study aimed to identify FA differences in low- and high-density lipoprotein (LDL and HDL, respectively) among young Spanish individuals with FH, treated as per guidelines recommendations, compared to their unaffected relatives with similar LDL concentrations in plasma. We also evaluated associations between the occurrence of cardiovascular event (CVE), dietary patterns, and the lipoprotein FA profile in FH. Methods: Lipoprotein FA profiles were determined by liquid chromatography/mass spectrometry/mass spectrometry (LC/MS/MS). Results: In comparison to their non-FH relatives, FH patients showed changes in the FA profile, predominantly in LDL particles while HDL particles were only modestly changed. FH individuals exhibited higher concentrations of poly- and monounsaturated FAs, oleic, γ-linoleic, α-linoleic, arachidonic, and eicosapentaenoic acids (p < 0.05). Interestingly, FH individuals showed greater adherence to the Mediterranean diet than their non-FH relatives, with no significant differences between those with and without previous CVE. The most pronounced changes in FA profile were observed in FH patients with a history of CVE, although the event itself did not significantly modify lipoprotein FA profiles. Conclusions: Well treated FH patients showed a FA profile that responded to a healthier diet than their relatives with similar plasma LDL levels. The strict lifestyle and pharmacological treatment affected positively the lipoproteins of FH patients and needs to be recommended.
HDL function and composition in atherothrombotic cardiovascular disease with very high HDL-C Teresa Padro, Natàlia Muñoz‐García, Marta Fanlo‐Maresma, Virginia Esteve‐Luque, Paula Cabré‐Fernandez, et al. European Journal of Clinical Investigation, 2026 Background Emerging evidence demonstrates a J‐shaped relationship between HDL‐C levels and atherosclerotic cardiovascular disease (ASCVD) with very high HDL‐C concentrations paradoxically associated with increased ASCVD events. This study aims to determine whether individuals with very high HDL‐C (>80 mg/dL) and ASCVD exhibit altered HDL composition and impaired HDL functionality. Methods We investigated the HDL profile and functionality in 49 subjects (mean age: 62 ± 2 years, 83% female) with very high HDL‐C levels (>80 mg/dL), including 23 with ASCVD. All ASCVD patients and 46% of those without ASCVD (non‐ASCVD) were on lipid‐lowering treatment. Results Plasma atherogenic lipoprotein‐cholesterol levels were significantly lower in ASCVD patients than in those without ASCVD, despite matched HDL‐C levels. CEC differences were evident after tertile stratification, with ASCVD participants overrepresented in the lowest tertile and showing lower median [IQR] CEC than non‐ASCVD ( p = 0.030). Total radical‐trapping antioxidative potential showed no significant group differences in HDL ability to inhibit copper‐induced LDL oxidation. However, basal HDL oxidative level was significantly higher in the ASCVD compared with the non‐ASCVD group ( p = 0.007). Inflammatory glycoproteins were inversely associated with CEC and HDL‐C levels in ASCVD patients, but not in non‐ASCVD patients. By NMR, mean HDL particle diameter did not differ between groups, yet ASCVD patients had fewer percent of large HDL particles compared to the non‐ASCVD (0.84 ± 0.02% vs. 0.91 ± 0.02%; p = 0.034) and a trend toward more small particles. HDL‐C content increased with particle size in ASCVD ( p = 0.008; r = 0.531), but not in non‐ASCVD, while HDL‐TG levels did not differ across tertiles. Functional cell‐based assays showed attenuated endothelial proliferation (normalized Cell‐Index) in ASCVD compared with non‐ASCVD, most evident in the largest HDL particle tertile. Conclusions These findings suggest that HDL functionality and particle distribution may offer more clinically relevant insights into cardiovascular risk than plasma HDL‐C concentrations alone, particularly in individuals with very high HDL‐C levels.
Atherogenic dyslipidaemia and residual cardiovascular risk: Understanding the link to heart disease Gabriela O. Girón, Sergi Otero, Panagiota Efstathia Nikolaou, Sebastià Alcover, Lisaidy Ramos‐Regalado, et al. European Journal of Clinical Investigation, 2026 Background A significant proportion of patients continue to experience cardiovascular (CV) events despite achieving recommended low‐density lipoprotein cholesterol (LDL‐C) targets, a phenomenon referred to as residual CV risk. Methods Clinical evidence from large outcome trials highlights the impact of residual risk on cardiovascular disease (CVD) burden, underscoring the need for therapeutic strategies beyond LDL‐C lowering. Residual CV risk arises from diverse mechanisms, including persistent atherogenic dyslipidaemia [elevated triglyceride‐rich lipoproteins (TRL), high triglycerides (TG), low high‐density lipoprotein cholesterol (HDL‐C) levels and increased apolipoprotein B (ApoB), Lipoprotein(a) (Lp[a]) and non‐HDL‐C], chronic inflammation, metabolic disorders and a prothrombotic state. These abnormalities continue to drive atherosclerotic progression in optimally treated patients, underscoring that managing residual CV risk requires a multifaceted approach. Results Lifestyle and dietary interventions remain foundational, targeting weight reduction, smoking cessation or adoption of a Mediterranean diet. Pharmacological options include statins (as first‐line therapy), or the use of ezetimibe, or bempedoic acid since they both have complementary effects to LDL‐C lowering. Emerging therapies, including proprotein convertase subtilisin/kexin type 9 (PCSK9), apolipoprotein C‐III (ApoC3) and angiopoietin‐like 3 (ANGPTL3) inhibitors, demonstrate potential efficacy in favourably modulating lipid profiles and targeting specific components of atherogenic dyslipidaemia (AD). Combination therapies tailored to individual lipid profiles show promise to reduce residual CV risk. Conclusion The following review aims to provide a comprehensive overview of the latest evidence on the factors driving residual CV risk and the therapeutic interventions available to treat atherogenic dyslipidaemia beyond LDL‐C reduction.
Gene Expression Pattern Associated with Cytoskeletal Remodeling in Lipid-Loaded Human Vascular Smooth Muscle Cells: Crosstalk Between C3 Complement and the Focal Adhesion Protein Paxillin Maisa Garcia-Arguinzonis, Rafael Escate, Roberta Lugano, Esther Peña, Maria Borrell-Pages, et al. Cells, 2025 Mechanical and contractile forces in the vascular wall regulate smooth muscle cell migration. We previously demonstrated the presence of C3 complement products in atherosclerotic lesions of human aortas and showed that that C3-derived fragments promote key cellular processes, such as actin cytoskeleton organization and cell migration, in lipid-loaded human vascular smooth muscle cells (hVSMCs). In the present study, we aimed to investigate gene expression profiles related to cytoskeletal remodeling and cell adhesion in migrating hVSMCs with a particular focus on modulatory effect of the C3 complement pathway on these processes. We analyzed gene expression in migrating and non-migrating hVSMCs using real-time PCR and in silico network analysis. Additionally, we investigated cytoskeletal remodeling through Western blotting and confocal microscopy. PCR profiling revealed 30 genes with significantly altered expression in migrating hVSMCs compared to non-migrating control cells. In silico analysis identified six of these genes—PXN, AKT1, RHOA, VCL, CTNNB1, and FN1—as being associated with cytoskeletal remodeling and focal adhesion, with PXN occupying a central position in the interaction network. PXN expression was reduced at both the transcript and protein levels and showed altered subcellular localization in migrating lipid-loaded hVSMCs. Protein–protein interaction analysis using STRING predicted an association between PXN and the integrin complex αMβ2 (comprising ITGAM (CD11b) and ITGB2 (CD18)), which functions as receptors for the iC3b complement fragment. Confocal imaging of cell adhesion structures revealed that lipid-loaded hVSMCs stimulated with iC3b displayed a more diffuse PXN distribution and significantly increased PXN–F-actin colocalization in active cytoplasmic regions compared to lipid-loaded control cells. PXN–F-actin colocalization increased from 1.26% to 19.68%. Subcellular fractionation further confirmed enhanced PXN enrichment in the membrane fraction, with no significant changes observed in the cytosolic or cytoskeletal compartments. In conclusion, iC3b-mediated molecular signaling in lipid-loaded hVSMCs alters PXN distribution and enhances cytoskeletal remodeling, revealing novel molecular interactions in vascular remodeling and the progression of atherosclerotic lesions.
Blood CD45+/CD3+ lymphocyte-released extracellular vesicles and mortality in hospitalized patients with coronavirus disease 2019 Rosa Suades, Maria F. Greco, Teresa Padró, Victoria de Santisteban, Pere Domingo, et al. European Journal of Clinical Investigation, 2025 BackgroundThe global pandemic of coronavirus disease 2019 (COVID‐19) represented a major public health concern. Growing evidence shows that plasma of COVID‐19 patients contains large numbers of circulating extracellular vesicles (cEVs) that correlate with disease severity and recovery. In this study, we sought to characterize the longitudinal cEV signature in critically ill COVID‐19 patients during hospitalization and its relation to mortality risk.MethodscEVs were quantitatively and phenotypically analysed in hospitalized non‐surviving COVID‐19 patients at baseline (n = 42) and before exitus (n = 40) and in 40 healthy volunteers as a reference group by high sensitivity nano flow cytometry using specific markers for parental cell sources and activation.ResultsLevels of cEV subtypes differed between patients with severe COVID‐19 and healthy subjects, specifically those from platelets and endothelial, inflammatory and viral infected cells, which associate to high mortality risk. In the longitudinal analysis from baseline to the time point immediately preceding death, no changes were found for platelet, pan‐leukocyte, and lung epithelial cell‐shed cEVs, while endothelial cell releases of EVs (eEVs) significantly differed. Vascular endothelial growth factor receptor 2‐positive eEVs were significantly increased before death compared to admission whereas endoglin and E‐selectin‐containing eEVs did not change. Conversely, lymphocyte (ℓEV), monocyte, macrophage, pericyte and progenitor cell‐derived cEVs displayed significant reductions before exitus. Noteworthy, levels of CD45+/CD3+‐ℓEVs were significantly associated to the patient's survival time.ConclusionsAn evolving cEV profile able to discriminate prompt risk of death during hospitalization has been defined suggesting a role for circulating and vascular cell‐derived EVs in COVID‐19 pathogenesis.
Endothelial Progenitor Cell Function in Patients With Coronary Chronic Total Occlusion and its Relationship With Collateral Circulation Journal of Invasive Cardiology, 2021
Endotoxin induction of plasminogen activator and plasminogen activator inhibitor type 1 mRNA in rat tissues in vivo Journal of Biological Chemistry, 1990
Distribution of tissue-type plasminogen activator (activity and antigen) in rat tissues. Blood Coagulation Fibrinolysis an International Journal in Haemostasis and Thrombosis, 1990
GRANT DETAILS
principal investigator and co-investigator of more than 50 research projects at Spanish level (regularly funded by the National Institute of Health and the Ministry of Science and Innovation - e.g. FIS, DTS, CDTI, RETOS among others -), within the European framework (IMI-JU: SAFE-T, TRansBioline; FP7: BiomarCare; H2020: COVIRNA; and others: EU CARDIOPATCH -SOE4/P1/E1063; International joint programming projects 2020: ERA-CVD/ AC20/00054; NextGeneration EU Project PLEC2021- 007664), and also funded by other public and privent entities (MATRATO TV· among other) and industry. She participates as investigator in Spanish-collaboration networks (CIBER, TERCEL, RICORS-TERAV) and she is also involved in scientific projects with transfer capacity (co-investigator of 3 patents and co-founder of 3 spin-offs)
RESEARCH OUTPUTS (PATENTS, SOFTWARE, PUBLICATIONS, PRODUCTS)
