Lucía Tejedor-Santamaría

ORCID: 0000-0003-4295-7284
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About
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Research Areas
  • Connective Tissue Growth Factor Research
  • Renal Diseases and Glomerulopathies
  • Complement system in diseases
  • Protein Degradation and Inhibitors
  • Biomarkers in Disease Mechanisms
  • Genetic and Kidney Cyst Diseases
  • Vitamin D Research Studies
  • Phagocytosis and Immune Regulation
  • Psoriasis: Treatment and Pathogenesis
  • Vitamin C and Antioxidants Research
  • Asthma and respiratory diseases
  • interferon and immune responses
  • Dialysis and Renal Disease Management
  • Histone Deacetylase Inhibitors Research
  • Acute Kidney Injury Research
  • Immune Cell Function and Interaction
  • Chronic Kidney Disease and Diabetes
  • Immune cells in cancer
  • TGF-β signaling in diseases
  • Acute Lymphoblastic Leukemia research
  • GDF15 and Related Biomarkers
  • IL-33, ST2, and ILC Pathways
  • Multiple Myeloma Research and Treatments
  • S100 Proteins and Annexins
  • Vascular Malformations and Hemangiomas

Hospital Universitario Fundación Jiménez Díaz
2019-2025

Instituto de Salud Carlos III
2020-2025

Universidad Autónoma de Madrid
2020-2025

Escuela Nacional de Sanidad
2025

Spanish Clinical Research Network
2021-2022

Chronic kidney disease (CKD) can be considered as a clinical model for premature aging. However, non-invasive biomarkers to detect early damage and the onset of senescent phenotype are lacking. Most preclinical senescence studies in aging have been done very old mice. Furthermore, precise characterization over-time development age-related remain unclear. To address these limitations, activation cellular senescence-associated mechanisms their correlation with structural changes were...

10.3390/antiox11020301 article EN cc-by Antioxidants 2022-01-31

Acute kidney injury (AKI) is more frequent in elderly patients. Mechanisms contributing to AKI (tubular cell death, inflammatory infiltration, impaired mitochondrial function, and prolonged cell-cycle arrest) have been linked cellular senescence, a process implicated regeneration failure progression fibrosis. However, the molecular pathological basis of age-related increase incidence not completely understood. To explore these mechanisms, experimental was induced by folic acid (FA)...

10.3389/fphar.2021.662020 article EN cc-by Frontiers in Pharmacology 2021-06-22

Chronic allograft dysfunction with progressive fibrosis of unknown cause remains a major issue after kidney transplantation, characterized by ischemia-reperfusion injury (IRI). One hypothesis to account for this is that spontaneous tubulointerstitial following IRI driven cellular senescence evolving from prolonged, unresolved DNA damage response (DDR). Since communication network factor 2 ((CCN2), formerly called connective tissue growth factor), an established mediator fibrosis, also...

10.1016/j.kint.2022.06.030 article EN cc-by Kidney International 2022-07-31

Background/Objectives: Acute kidney injury (AKI) remains an unsolved medical problem due to the lack of effective treatments, high mortality and increased susceptibility progression chronic disease (CKD), especially in elderly. Cellular senescence has been described AKI, CKD ageing, proposed as a promising therapeutic target. The senolytic drugs combination dasatinib plus quercetin (D&Q) is beneficial some pathological conditions, including experimental CKD, but there no data AKI....

10.20944/preprints202504.2175.v1 preprint EN 2025-04-25

Cellular communication network factor 2 (CCN2, also known as CTGF) is a complex protein that regulates numerous cellular functions. This biomolecule exhibits dual functions, depending on the context, and can act matricellular or growth factor. CCN2 an established marker of fibrosis well-known mediator kidney damage, involved in regulation inflammation, extracellular matrix remodeling, cell death, activation tubular epithelial (TECs) senescence. In response to senescence mechanisms are...

10.3390/ijms26094401 article EN International Journal of Molecular Sciences 2025-05-06

Background/Objectives: Acute kidney injury (AKI) remains an unsolved medical problem due to the lack of effective treatments, high mortality, and increased susceptibility progression chronic disease (CKD), especially in elderly. Cellular senescence has been described AKI, CKD, aging proposed as a promising therapeutic target. The senolytic drug combination dasatinib plus quercetin (D&Q) is beneficial some pathological conditions, including experimental but there are no data for AKI....

10.3390/ph18060822 article EN cc-by Pharmaceuticals 2025-05-30

Crescentic glomerulonephritis is a devastating autoimmune disease that without early and properly treatment may rapidly progress to end-stage renal death. Current immunosuppressive provides limited efficacy an important burden of adverse events. Epigenetic drugs are source novel therapeutic tools. Among them, bromodomain extraterminal domain (BET) inhibitors (iBETs) block the interaction between bromodomains acetylated proteins, including histones transcription factors. iBETs have...

10.3390/ph15020121 article EN cc-by Pharmaceuticals 2022-01-20

Inflammation is a key characteristic of both acute and chronic kidney diseases. Preclinical data suggest the involvement NLRP3/Inflammasome, receptor-interacting protein kinase-3 (RIPK3), NRF2/oxidative pathways in regulation inflammation. Cellular communication network factor 2 (CCN2, also called CTGF past) an established fibrotic biomarker well-known mediator damage. CCN2 was shown to be involved damage through proinflammatory profibrotic responses. However, date, potential role...

10.3390/antiox12081541 article EN cc-by Antioxidants 2023-07-31

Cellular communication network-2 (CCN2), also called connective tissue growth factor (CTGF), is considered a fibrotic biomarker and has been suggested as potential therapeutic target for kidney pathologies. CCN2 matricellular protein with four distinct structural modules that can exert dual function factor. Previous experiments using surface plasmon resonance cultured renal cells have demonstrated the C-terminal module of (CCN2(IV)) interacts epidermal receptor (EGFR). Moreover, CCN2(IV)...

10.3390/biom12020252 article EN cc-by Biomolecules 2022-02-03

The cellular communication network factor 2 (CCN2/CTGF) has been traditionally described as a mediator of the fibrotic responses induced by other factors including transforming growth β (TGF-β). However, several studies have defined direct role CCN2 acting inducing oxidative and proinflammatory responses. presence TGF-β together in context requisite to induce persistent response, but precise mechanisms implicated this relation are not yet. Considering main receptors (TβR) pathway activation,...

10.3390/ijms23010375 article EN International Journal of Molecular Sciences 2021-12-29

Peritoneal dialysis (PD) is a current replacement therapy for end-stage kidney diseases (ESKDs). However, long-term exposure to PD fluids may lead damage of the peritoneal membrane (PM) through mechanisms involving activation inflammatory response and mesothelial-to-mesenchymal transition (MMT), leading filtration failure. depends on complex interaction among external stimuli, intrinsic properties PM, subsequent activities local innate–adaptive immune system. Epigenetic drugs targeting...

10.3390/antiox12122055 article EN cc-by Antioxidants 2023-11-29

Cellular Communication Network Factor 2 (CCN2) is a matricellular protein implicated in cell communication and microenvironmental signaling. Overexpression of CCN2 has been documented various cardiovascular pathologies, wherein it may exert either deleterious or protective effects depending on the pathological context, thereby suggesting that its role system not yet fully elucidated. In this study, we aimed to investigate

10.3390/ijms25179617 article EN International Journal of Molecular Sciences 2024-09-05

Abstract Peritoneal dialysis (PD) is a widely used kidney replacement therapy for end-stage disease (ESKD) patients. However, long-term exposure to PD fluids (PDF) can lead peritoneal membrane (PM) damage, causing ultrafiltration failure and thus discontinuation. Investigating the molecular mechanisms underlying this damage crucial identifying new therapeutic targets mitigate deterioration in Therefore, work we study role of STING inflammation fibrosis. To aim, performed different...

10.1101/2024.11.19.621845 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-11-21

Abstract Background and Aims Acute kidney injury (AKI) is associated with elevated mortality morbidity presenting higher frequency in aged patients. Different mechanisms are activated AKI, including tubular epithelial cell death (apoptosis regulated necrosis), inflammatory infiltration, impaired mitochondrial function, prolonged cell-cycle arrest (or cellular senescence). There a strong connection between pathways AKI development of senescence, process implicated regeneration failure...

10.1093/ndt/gfab084.0011 article EN Nephrology Dialysis Transplantation 2021-05-01

Crescentic glomerulonephritis is a devastating autoimmune disease that without early and properly treat-ment may rapidly progress to end-stage renal death. Current immunosuppressive treatment provided limited efficacy an important burden of adverse events. Epigenetic drugs are source novel therapeutic tools. Among them, bromodomain extraterminal domain (BET) inhibitors (iBETs) block the interaction between bromodomains acetylated proteins, including histones transcription factors. iBETs have...

10.20944/preprints202112.0290.v2 preprint EN 2021-12-20
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