Silvia Affò

ORCID: 0000-0002-9731-3913
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About
Contact & Profiles
Research Areas
  • Liver Disease Diagnosis and Treatment
  • Liver physiology and pathology
  • Alcohol Consumption and Health Effects
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Pancreatic and Hepatic Oncology Research
  • Liver Disease and Transplantation
  • Diet, Metabolism, and Disease
  • Hepatitis C virus research
  • Pediatric Hepatobiliary Diseases and Treatments
  • Organ Transplantation Techniques and Outcomes
  • MicroRNA in disease regulation
  • Peptidase Inhibition and Analysis
  • Cancer-related molecular mechanisms research
  • Hippo pathway signaling and YAP/TAZ
  • Bone and Dental Protein Studies
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Cancer-related gene regulation
  • Fibroblast Growth Factor Research
  • Pancreatitis Pathology and Treatment
  • Cancer Cells and Metastasis
  • Genetic factors in colorectal cancer
  • Endoplasmic Reticulum Stress and Disease
  • Phagocytosis and Immune Regulation
  • Pancreatic function and diabetes
  • Traumatic Brain Injury and Neurovascular Disturbances

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer
2013-2025

Fundació Clínic per a la Recerca Biomèdica
2023

Fundació de Recerca Clínic Barcelona-Institut d’Investigacions Biomèdiques August Pi i Sunyer
2023

Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas
2011-2022

Columbia University
2013-2022

Universitat de Barcelona
2014-2015

Hospital Clínic de Barcelona
2015

Inova Health System
2013

Edinburgh Royal Infirmary
2013

University of Liverpool
2013

Alcoholic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death. However, the driving factors are largely unknown. At admission, patients with AH often show criteria of systemic inflammatory response syndrome (SIRS) even in absence an infection. We hypothesize that presence SIRS may predispose MOF To test this hypothesis, we studied a cohort including 162 biopsy‐proven AH. The infections was assessed all patients, multivariate analyses identified variables...

10.1002/hep.27779 article EN Hepatology 2015-03-11

Cancer-associated fibroblasts (CAF) may exert tumor-promoting and tumor-suppressive functions, but the mechanisms underlying these opposing effects remain elusive. Here, we sought to understand potentially functions by interrogating functional relationships among CAF subtypes, their mediators, desmoplasia, tumor growth in a wide range of types metastasizing liver, most common organ site for metastasis. Depletion hepatic stellate cells (HSC), which represented main source mice patients our...

10.1172/jci146987 article EN Journal of Clinical Investigation 2021-04-27

In many organs, including the intestine and skin, cancers originate from cells of stem or progenitor compartment. Despite its nomenclature, cellular origin hepatocellular carcinoma (HCC) remains elusive. contrast to most liver lacks a defined cell population for organ maintenance. Previous studies suggest that both hepatocytes facultative within biliary compartment are capable generating HCC. As HCCs with signature carry worse prognosis, understanding HCC is clinical relevance. Here, we used...

10.1172/jci77995 article EN Journal of Clinical Investigation 2015-09-07

Objective The diversity of the tumour microenvironment (TME) intrahepatic cholangiocarcinoma (iCCA) has not been comprehensively assessed. We aimed to generate a novel molecular iCCA classifier that incorporates elements stroma, and immune (‘STIM’ classification). Design applied virtual deconvolution transcriptomic data from ~900 iCCAs, enabling us devise classification by selecting for most relevant TME components. Murine models were generated through hydrodynamic tail vein injection...

10.1136/gutjnl-2021-326514 article EN Gut 2022-05-18

<h3>Objective</h3> Alcoholic hepatitis (AH) is a severe clinical condition that needs novel therapies. The identification of targets for therapy hampered by the lack animal models advanced AH. authors performed translational study through transcriptome analysis in patients with AH to identify new molecular targets. <h3>Design</h3> Hepatic gene expression profiling was assessed DNA microarray (n=15) and normal livers (n=7). Functional set enrichment analysis. Quantitative PCR (n=40), C...

10.1136/gutjnl-2011-301146 article EN Gut 2012-05-25

Severe liver diseases are characterized by expansion of progenitor cells (LPC), which correlates with disease severity. However, the origin and role LPC in physiology hepatic injury remains a contentious topic. We found that ductular reaction human cirrhotic livers express hepatocyte nuclear factor 1 homeobox B (HNF1β). HNF1β expression was not present newly generated epithelial cell adhesion molecule (EpCAM)-positive hepatocytes. In order to investigate HNF1β-expressing we used...

10.1002/hep.27078 article EN Hepatology 2014-02-20

Objective Chemokines are known to play an important role in the pathophysiology of alcoholic hepatitis (AH), a form acute-on-chronic liver injury frequently mediated by gut derived lipopolysaccharide (LPS). In our study, we hypothesise that chemokine CCL20, one most upregulated chemokines patients with AH, is implicated pathogenesis AH mediating LPS induced injury. Design CCL20 gene expression and serum levels their correlation disease severity were assessed AH. Cellular sources its...

10.1136/gutjnl-2013-306098 article EN Gut 2014-01-10

Fibrosis contributes to ~45% of deaths in western countries. In chronic liver disease, fibrosis is a major factor determining outcomes, but efficient antifibrotic therapies are lacking. Although platelet-derived growth and transforming factor–β constitute key fibrogenic mediators, they do not account for the well-established link between cell death liver. Here, we hypothesized that damage-associated molecular patterns (DAMPs) may epithelial fibrogenesis injured DAMP receptor screening...

10.1126/scitranslmed.abe5795 article EN Science Translational Medicine 2022-04-06

Defining the trajectory of cells during differentiation and disease is key for uncovering mechanisms driving cell fate identity. However, trajectories human remain largely unexplored due to challenges studying them with samples. In this study, we investigate proteome iPSCs hepatic stellate (diHSCs) identify RORA as a transcription factor governing metabolic reprogramming HSCs necessary diHSCs' commitment, identity, activation. Using deficient pharmacologic interventions, show that required...

10.1038/s41467-025-56024-4 article EN cc-by-nc-nd Nature Communications 2025-02-10

We identified, in the transcriptome analysis of patients with alcoholic hepatitis (AH), osteopontin (OPN) as one most up-regulated genes. Here, we used a translational approach to investigate its pathogenic role. OPN hepatic gene expression was quantified AH and other liver diseases. protein processing were assessed by immmunohistochemistry, western blotting enzyme-linked immunosorbent assay. polymorphisms evaluated disease. The role OPN−/− mice alcohol-induced injury. biological actions...

10.1002/hep.26521 article EN Hepatology 2013-05-31

Abstract Unveiling the regulatory pathways maintaining hepatic stellate cells (HSC) in a quiescent (q) phenotype is essential to develop new therapeutic strategies treat fibrogenic diseases. To uncover miRNA-mRNA interactions qHSCs, HSCs were FACS-sorted from healthy livers and activated (aHSCs) generated vitro . MiRNA Taqman array analysis showed expressed low number of miRNAs (n = 259), which 47 down-regulated 212 up-regulated upon activation. Computational integration miRNA gene...

10.1038/srep11549 article EN cc-by Scientific Reports 2015-06-22

Fibrosis and cancer represent two major complications of chronic liver disease. MicroRNAs have been implicated in the development fibrosis cancer, thus constituting potential therapeutic targets. Here, we investigated role microRNA‐21 (miR‐21), a microRNA that has multiple organs also suggested to act as an “oncomir.” Accordingly, miR‐21 was showed strongest up‐regulation activated hepatic stellate cells (HSCs) models fibrogenesis, with 8‐fold 24‐fold induction compared quiescent HSCs....

10.1002/hep.29627 article EN Hepatology 2017-11-01
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