Águeda González‐Rodríguez

ORCID: 0000-0003-2851-2318
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Liver Disease Diagnosis and Treatment
  • Diet, Metabolism, and Disease
  • Pancreatic function and diabetes
  • Protein Tyrosine Phosphatases
  • Endoplasmic Reticulum Stress and Disease
  • Adipose Tissue and Metabolism
  • Liver physiology and pathology
  • Lipid metabolism and disorders
  • Drug-Induced Hepatotoxicity and Protection
  • Hepatitis C virus research
  • Autophagy in Disease and Therapy
  • Liver Disease and Transplantation
  • Diabetes and associated disorders
  • Alcohol Consumption and Health Effects
  • PI3K/AKT/mTOR signaling in cancer
  • Genomics, phytochemicals, and oxidative stress
  • Metabolism, Diabetes, and Cancer
  • Diet and metabolism studies
  • MicroRNA in disease regulation
  • Drug Transport and Resistance Mechanisms
  • Galectins and Cancer Biology
  • Lipid metabolism and biosynthesis
  • Adipokines, Inflammation, and Metabolic Diseases
  • Retinal Diseases and Treatments
  • Obstructive Sleep Apnea Research

Universidad Autónoma de Madrid
2011-2025

Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas
2012-2025

Instituto de Investigaciones Biomédicas Sols-Morreale
2010-2025

Consejo Superior de Investigaciones Científicas
2008-2025

Instituto de Salud Carlos III
2014-2024

Hospital Universitario Santa Cristina
2016-2023

Universitat de Barcelona
2023

University Hospital Mútua de Terrassa
2022-2023

Mútua Terrassa
2023

Universitat Autònoma de Barcelona
2023

The pathogenic mechanisms underlying the progression of non-alcoholic fatty liver disease (NAFLD) are not fully understood. In this study, we aimed to assess relationship between endoplasmic reticulum (ER) stress and autophagy in human mouse hepatocytes during NAFLD. ER markers were analyzed livers from patients with biopsy-proven steatosis (NAS) or steatohepatitis (NASH) compared subjects histologically normal liver, mice fed chow diet (CHD) high fat (HFD) methionine-choline-deficient (MCD)...

10.1038/cddis.2014.162 article EN cc-by Cell Death and Disease 2014-04-17

Sirtuin 1 (SIRT1) is a key player in liver physiology and therapeutic target against hepatic inflammation. We evaluated the role of SIRT1 proinflammatory context oxidative stress during acetaminophen (APAP)-mediated hepatotoxicity.SIRT1 protein levels decreased human mouse livers following APAP overdose. SIRT1-Tg mice maintained higher on injection than wild-type were protected hepatotoxicity by modulation antioxidant systems restrained inflammatory responses, with stress, cytokine messenger...

10.1089/ars.2017.7373 article EN Antioxidants and Redox Signaling 2017-10-31

Retinal neurodegeneration is an early event in the pathogenesis of diabetic retinopathy (DR). Somatostatin (SST) endogenous neuroprotective peptide that downregulated eye. The aim study was to test usefulness topical administration SST preventing retinal neurodegeneration. For this purpose, rats with streptozotocin-induced diabetes mellitus (STZ-DM) were treated either eye drops or vehicle for 15 days. Nondiabetic served as a control group. Functional abnormalities assessed by...

10.2337/db12-0926 article EN cc-by-nc-nd Diabetes 2013-03-09

Nonalcoholic fatty liver disease (NAFLD) is considered the next major health epidemic with an estimated 25% worldwide prevalence. No drugs have yet been approved and NAFLD remains a unmet need. Here, we identify MCJ (Methylation-Controlled J protein) as target for non-alcoholic steatohepatitis (NASH), advanced phase of NAFLD. endogenous negative regulator respiratory chain Complex I that acts to restrain mitochondrial respiration. We show therapeutic targeting in nanoparticle-...

10.1038/s41467-020-16991-2 article EN cc-by Nature Communications 2020-07-03

Because nonalcoholic steatohepatitis (NASH) is associated with impaired liver regeneration, we investigated the effects of G49, a dual glucagon‐like peptide‐1/glucagon receptor agonist, on NASH and hepatic regeneration. C57Bl/6 mice fed chow or methionine choline–deficient (MCD) diet for 1 week were divided into 4 groups: control (chow diet), MCD diet, plus M+G49 (MCD G49). Mice high‐fat (HFD) 10 weeks HFD H+G49 (HFD Following 2 groups) 3 treatment partial hepatectomy (PH) was performed, all...

10.1002/hep.28962 article EN Hepatology 2016-11-23

Non-alcoholic steatohepatitis (NASH) is a common chronic liver disease that compromises function, for which there not specifically approved medicine. Recent research has identified transcription factor NRF2 as potential therapeutic target. However, current activators, designed to inhibit its repressor KEAP1, exhibit unwanted side effects. Alternatively, we previously introduced PHAR, protein-protein interaction inhibitor of NRF2/β-TrCP, induces mild activation and selectively activates in...

10.1016/j.redox.2024.103027 article EN cc-by-nc-nd Redox Biology 2024-01-03

OBJECTIVE Mice with complete deletion of insulin receptor substrate 2 (IRS2) develop hyperglycemia, impaired hepatic signaling, and elevated gluconeogenesis, whereas mice deficient for protein tyrosine phosphatase (PTP)1B display an opposing phenotype characterized by increased sensitivity to insulin. To define the relationship between these two signaling pathways in regulation liver metabolism, we used genetic pharmacological approaches study effects inhibiting PTP1B on expression...

10.2337/db09-0796 article EN cc-by-nc-nd Diabetes 2009-12-22

Bacterial LPS (endotoxin) has been implicated in the pathogenesis of acute liver disease through its induction proinflammatory cytokine TNF-α. TNF-α is a key determinant outcome well-established mouse model failure during septic shock. One possible mechanism for regulating expression control protein elongation translation, which would allow rapid cell adaptation to physiological changes. However, regulation translational poorly understood. We found that p38γ/δ MAPK proteins required nascent...

10.1172/jci65124 article EN Journal of Clinical Investigation 2012-12-03

Summary Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of insulin signaling and therapeutic target for type 2 diabetes (T2DM). In this study, we have evaluated the role PTP1B in development aging‐associated obesity, inflammation, peripheral resistance by assessing metabolic parameters at 3 16 months −/− mice maintained on mixed genetic background (C57Bl/6J × 129Sv/J). Whereas fat mass adipocyte size were increased wild‐type control months, these did not change with aging...

10.1111/j.1474-9726.2011.00786.x article EN other-oa Aging Cell 2011-12-29

Acute hepatic failure secondary to acetaminophen (APAP) poisoning is associated with high mortality. Protein tyrosine phosphatase 1B (PTP1B) a negative regulator of kinase growth factor signaling. In the liver, this pathway confers protection against injury. However, involvement PTP1B in intracellular networks activated by APAP unknown. We have assessed expression APAP-induced liver humans and its role molecular mechanisms that regulate balance between cell death survival human mouse...

10.1038/cddis.2013.150 article EN cc-by Cell Death and Disease 2013-05-09

Inhibition of protein tyrosine phosphatase 1B (PTP1B) has been suggested as an attractive target to improve insulin sensitivity in different cell types. In the present work, we have investigated effect PTP1B deficiency on response human and murine macrophages. Using vitro vivo approaches mice silencing macrophages with specific siRNAs, demonstrated that increases effects pro-inflammatory stimuli both rodent at time decreases alternative stimulation. Moreover, absence induces a loss viability...

10.1038/cddis.2014.90 article EN cc-by Cell Death and Disease 2014-03-13

Background and Aims G protein–coupled receptor (GPR) 55 is a putative cannabinoid receptor, l‐α‐lysophosphatidylinositol (LPI) its only known endogenous ligand. Although GPR55 has been linked to energy homeostasis in different organs, specific role lipid metabolism the liver contribution pathophysiology of nonalcoholic fatty disease (NAFLD) remains unknown. Approach Results We measured (1) expression patients with NAFLD compared individuals without obesity disease, as well animal models...

10.1002/hep.31290 article EN cc-by-nc Hepatology 2020-04-24

In this study, we found an imbalance between stress-mediated and survival signaling elevated apoptotic markers in retinal pigment epithelium (RPE) from diabetic patients. Since fenofibric acid (FA) treatment reduces the progression of retinopathy (DR), investigated effect hyperglycemia hypoxia, two components milieu, on stress, apoptosis, pathways ARPE-19 cells (immortalized human RPE cell line) whether FA is able to prevent deleterious effects induced by these conditions. cultured...

10.1002/jcp.22970 article EN Journal of Cellular Physiology 2011-08-08

Mice with deletion of insulin receptor substrate (IRS) 2 develop hyperglycaemia, impaired hepatic signaling and elevated gluconeogenesis. Protein tyrosine phosphatase 1B (PTP1B) inhibition by resveratrol improves peripheral sensitivity these mice. Although activates Sirtuin1 (Sirt1), the mechanisms underlying its beneficial effects are not totally elucidated. In this study, we have investigated whether Sirt1 mediates in controlling resistance diabetic mice.We attempted to ameliorate two...

10.1002/mnfr.201400933 article EN Molecular Nutrition & Food Research 2015-03-25

Different data support a role for the epidermal growth factor receptor (EGFR) pathway during liver regeneration and hepatocarcinogenesis. However, important issues, such as precise mechanisms mediating its actions unique versus redundant functions, have not been fully defined. Here, we present novel transgenic mouse model expressing hepatocyte‐specific truncated form of human EGFR, which acts negative dominant mutant (ΔEGFR) allows definition tyrosine kinase–dependent functions. Results...

10.1002/hep.28134 article EN Hepatology 2015-08-27

Autophagy-related gene 3 (ATG3) is an enzyme mainly known for its actions in the LC3 lipidation process, which essential autophagy. Whether ATG3 plays a role lipid metabolism or contributes to non-alcoholic fatty liver disease (NAFLD) remains unknown.By performing proteomic analysis on livers from mice with genetic manipulation of hepatic p63, regulator acid metabolism, we identified as new target downstream p63. was evaluated samples patients NAFLD. Further, performed human hepatocyte cell...

10.1016/j.jhep.2021.09.008 article EN cc-by-nc-nd Journal of Hepatology 2021-09-21

Accumulation evidence links obesity-induced inflammation as an important contributor to the development of insulin resistance, which plays a key role in pathophysiology obesity-related diseases such type 2 diabetes and nonalcoholic fatty liver disease. Cyclooxygenase (COX)-1 -2 catalyze first step prostanoid biosynthesis. Because adult hepatocytes fail induce COX-2 expression regardless proinflammatory stimuli used, we have evaluated whether this lack under mild conditions might constitute...

10.2337/db14-0979 article EN Diabetes 2014-11-24
Coming Soon ...