Biochemistry, Genetics and Molecular Biology, Physiology, Molecular Medicine, Endocrinology
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Scopus Publications
Type 2 diabetes risk alleles in peptidyl-glycine alpha-amidating monooxygenase influence GLP-1 levels and response to GLP-1 receptor agonists Mahesh M. Umapathysivam, Elisa Araldi, Benoit Hastoy, Adem Y. Dawed, Hasan Vatandaslar, Johanna E. Mayrhofer, Peter Lindquist, Pamuditha N. Silva, Algera Goga, Geraldine O. Trüllinger, Svenja Godbersen, Shahana Sengupta, Adrian Kaufmann, Søren Krogsgaard Thomsen, Bolette Hartmann, Yi-Chun Chen, Anna E. Jonsson, Hasan Kabakci, Swaraj Thaman, Niels Grarup, Christian T. Have, Lindsay P. Pallo, Kristine Faerch, Anette P. Gjesing, Sameena Nawaz, Jane Cheeseman, Matthew J. Neville, Oluf Pedersen, Mark Walker, Han Sun, Christopher Jennison, Andrew T. Hattersley, Jens F. Rehfeld, Rury R. Holman, Bruce C. Verchere, Torben Hansen, Fredrik Karpe, Jens J. Holst, Mette M. Rosenkilde, Angus G. Jones, Michael Ristow, Mark I. McCarthy, Ewan R. Pearson, Markus Stoffel, Anna L. Gloyn Genome Medicine, 2026 BACKGROUND: Type 2 diabetes (T2D) is a leading cause of morbidity and mortality worldwide. Despite the availability of multiple glucose-lowering agents, only half of individuals with T2D achieve the recommended HbA1c target of < 7.0%. Precision medicine approaches that leverage patient-specific markers offer a promising strategy to improve therapeutic outcomes. The PAM gene encodes the sole enzyme responsible for amidating bioactive hormones, including GLP-1, and harbors two hypomorphic T2D-risk alleles (p.D563G and p.S539W); however, whether PAM regulates GLP-1, a key amidated incretin hormone, and whether this influences response to GLP-1 receptor agonist (GLP-1RA) therapy, remains unknown. METHODS: PAM amidation activity, postprandial GLP-1 levels, and the incretin effect were measured in carriers of PAM T2D-risk alleles and matched non-carriers from the Oxford Biobank in a prospective observational study and in Danish cohorts. Inducible whole-body Pam knockout mice were generated; gastric emptying was assessed by paracetamol absorption assay with and without exendin-4. Glycemic response to GLP-1RAs was evaluated in a meta-analysis of 1,119 participants across three cohorts (IMI-DIRECT, GoDARTS, PRIBA), with comparative assessment of sulphonylurea, metformin, and DPP-4 inhibitor response. RESULTS: Carriers of p.S539W and p.D563G alleles demonstrated 52% and 20% reductions in serum PAM amidation activity, respectively. Both human carriers and Pam knockout mice exhibited elevated circulating GLP-1 levels; however, p.S539W carriers showed an 18% reduction in endogenous GLP-1 sensitivity. PamKO mice displayed accelerated gastric emptying that was refractory to exendin-4, alongside impaired cAMP signaling downstream of the GLP-1 receptor in the pylorus. In the clinical meta-analysis, p.S539W carriers showed a significantly attenuated HbA1c reduction following GLP-1RA therapy (− 0.69% vs. − 1.24% in non-carriers; p = 0.025), representing a 44% relative loss of glycemic benefit; only 11.5% of carriers achieved HbA1c < 7% compared with 25.3% of non-carriers. No differences in response to sulphonylureas, metformin, or DPP-4 inhibitors were observed. CONCLUSIONS: Hypomorphic PAM T2D-risk alleles reduce amidating enzyme activity, elevate circulating GLP-1 levels, and impair GLP-1 post-receptor signaling, culminating in a selective and clinically meaningful reduction in GLP-1RA efficacy. These findings establish PAM genotype as a novel pharmacogenomic determinant of GLP-1RA response, supporting its incorporation into precision medicine frameworks to optimize drug selection in T2D management. TRIAL REGISTRATION: NCT02723110, NCT02465515 and NCT01144338.
Effect of Empagliflozin on the plasma lipidome in patients with type 2 diabetes mellitus: results from the EmDia clinical trial Katrin I. Bauer, Dhanwin Baker, Raissa Lerner, Thomas Koeck, Gregor Buch, Zlatka Fischer, Robin Martens, Ekaterina E. Esenkova, Maximilian Nuber, Miguel A. Andrade-Navarro, Vincent ten Cate, Stefan Tenzer, Philipp S. Wild, Laura Bindila, Elisa Araldi Cardiovascular Diabetology, 2025 Background Sodium-glucose cotransporter 2 (SGLT2) inhibitors, such as Empagliflozin, are antidiabetic drugs that reduce glucose levels and have emerged as a promising therapy for patients with heart failure (HF), although the exact molecular mechanisms underlying their cardioprotective effects remain to be fully elucidated. The EmDia study, a randomized, double-blind trial conducted at the University Medical Center of Mainz, has confirmed the beneficial effects of Empagliflozin in HF patients after both one and twelve weeks of treatment. In this work, we aimed to assess whether changes in lipid profiles driven by Empagliflozin use in HF patients in the EmDia trial could assist in gaining a better understanding of its cardioprotective mechanisms. Methods Lipid analysis of blood plasma from 144 patients from the EmDia trial was conducted using 4D-LC-TIMS/IMS lipidomics. Lipid signatures after treatment for one and twelve weeks, respectively, were obtained with sparse group LASSO regularized regression models. Linear regression models were employed to highlight associations between significantly changed clinical traits and lipids. Results The lipid signatures after one week of treatment consisted of 37 lipids from the lipid groups lysophosphatidylcholine (LPC), phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelin (SM), and triacylglycerol (TG). After twelve weeks, the signature comprised 24 lipids from the same five lipid groups, along with Ceramides (Cer). Three of five lipids altered at both time points showed consistent directional trends. Empagliflozin treatment led to significant alterations in the lipidome, including increases in both beneficial lipids, such as LPCs, and potentially harmful species, notably ceramides, which have been implicated in lipotoxicity and cardiovascular risk. Conclusion This study identified distinct lipid signatures associated with Empagliflozin treatment after both one and twelve weeks, respectively, with five lipids overlapping between signatures and three with consistent directions, revealing that some of the beneficial effects of Empagliflozin could be through lipid modulation. Notably, Empagliflozin-modulated lipids associated with changes in clinical traits and lipid-specific profiles among clinical subgroups were observed. However, challenges remain in establishing direct associations between individual lipids and clinical outcomes. Future research integrating lipidomics data with other omics datasets could provide a more comprehensive understanding of the identified lipid signatures and their potential roles in health and diseases. Trial registration ClinicalTrials.gov; NCT02932436. Registration date, 2016/10/13. Graphical abstract
A Map of the Lipid–Metabolite–Protein Network to Aid Multi-Omics Integration Uchenna Alex Anyaegbunam, Aimilia-Christina Vagiona, Vincent ten Cate, Katrin Bauer, Thierry Schmidlin, Ute Distler, Stefan Tenzer, Elisa Araldi, Laura Bindila, Philipp Wild, Miguel A. Andrade-Navarro Biomolecules, 2025 The integration of multi-omics data offers transformative potential for elucidating complex molecular mechanisms underlying biological processes and diseases. In this study, we developed a lipid–metabolite–protein network that combines a protein–protein interaction network and enzymatic and genetic interactions of proteins with metabolites and lipids to provide a unified framework for multi-omics integration. Using hyperbolic embedding, the network visualizes connections across omics layers, accessible through a user-friendly Shiny R (version 1.10.0) software package. This framework ranks molecules across omics layers based on functional proximity, enabling intuitive exploration. Application in a cardiovascular disease (CVD) case study identified lipids and metabolites associated with CVD-related proteins. The analysis confirmed known associations, like cholesterol esters and sphingomyelin, and highlighted potential novel biomarkers, such as 4-imidazoleacetate and indoleacetaldehyde. Furthermore, we used the network to analyze empagliflozin’s temporal effects on lipid metabolism. Functional enrichment analysis of proteins associated with lipid signatures revealed dynamic shifts in biological processes, with early effects impacting phospholipid metabolism and long-term effects affecting sphingolipid biosynthesis. Our framework offers a versatile tool for hypothesis generation, functional analysis, and biomarker discovery. By bridging molecular layers, this approach advances our understanding of disease mechanisms and therapeutic effects, with broad applications in computational biology and precision medicine.
A Systematic Review of Lipid-Focused Cardiovascular Disease Research: Trends and Opportunities Uchenna Alex Anyaegbunam, Piyush More, Jean-Fred Fontaine, Vincent ten Cate, Katrin Bauer, Ute Distler, Elisa Araldi, Laura Bindila, Philipp Wild, Miguel A. Andrade-Navarro Current Issues in Molecular Biology, 2023 Lipids are important modifiers of protein function, particularly as parts of lipoproteins, which transport lipophilic substances and mediate cellular uptake of circulating lipids. As such, lipids are of particular interest as blood biological markers for cardiovascular disease (CVD) as well as for conditions linked to CVD such as atherosclerosis, diabetes mellitus, obesity and dietary states. Notably, lipid research is particularly well developed in the context of CVD because of the relevance and multiple causes and risk factors of CVD. The advent of methods for high-throughput screening of biological molecules has recently resulted in the generation of lipidomic profiles that allow monitoring of lipid compositions in biological samples in an untargeted manner. These and other earlier advances in biomedical research have shaped the knowledge we have about lipids in CVD. To evaluate the knowledge acquired on the multiple biological functions of lipids in CVD and the trends in their research, we collected a dataset of references from the PubMed database of biomedical literature focused on plasma lipids and CVD in human and mouse. Using annotations from these records, we were able to categorize significant associations between lipids and particular types of research approaches, distinguish non-biological lipids used as markers, identify differential research between human and mouse models, and detect the increasingly mechanistic nature of the results in this field. Using known associations between lipids and proteins that metabolize or transport them, we constructed a comprehensive lipid–protein network, which we used to highlight proteins strongly connected to lipids found in the CVD-lipid literature. Our approach points to a series of proteins for which lipid-focused research would bring insights into CVD, including Prostaglandin G/H synthase 2 (PTGS2, a.k.a. COX2) and Acylglycerol kinase (AGK). In this review, we summarize our findings, putting them in a historical perspective of the evolution of lipid research in CVD.
Lithium treatment extends human lifespan: findings from the UK Biobank Elisa Araldi, Catherine R. Jutzeler, Michael Ristow Aging, 2023 Lithium is a nutritional trace element that is also used pharmacologically for the management of bipolar and related psychiatric disorders. Recent studies have shown that lithium supplementation can extend health and lifespan in different animal models. Moreover, nutritional lithium uptake from drinking water was repeatedly found to be positively correlated with human longevity. By analyzing a large observational aging cohort (UK Biobank, n = 501,461 individuals) along with prescription data derived from the National Health Services (NHS), we here find therapeutic supplementation of lithium linked to decreased mortality (p = 0.0017) of individuals diagnosed with affective disorders. Subsequent multivariate survival analyses reveal lithium to be the strongest factor in regards to increased survival effects (hazard ratio = 0.274 [0.119–0.634 CI 95%, p = 0.0023]), corresponding to 3.641 times lower (95% CI 1.577–8.407) chances of dying at a given age for lithium users compared to users of other anti-psychotic drugs. While these results may further support the use of lithium as a geroprotective supplement, it should be noted that doses applied within the UK Biobank/NHS setting require close supervision by qualified medical professionals.
Germline loss-of-function PAM variants are enriched in subjects with pituitary hypersecretion Giampaolo Trivellin, Adrian F. Daly, Laura C. Hernández-Ramírez, Elisa Araldi, Christina Tatsi, Ryan K. Dale, Gus Fridell, Arjun Mittal, Fabio R. Faucz, James R. Iben, Tianwei Li, Eleonora Vitali, Stanko S. Stojilkovic, Peter Kamenicky, Chiara Villa, Bertrand Baussart, Prashant Chittiboina, Camilo Toro, William A. Gahl, Erica A. Eugster, Luciana A. Naves, Marie-Lise Jaffrain-Rea, Wouter W. de Herder, Sebastian JCMM Neggers, Patrick Petrossians, Albert Beckers, Andrea G. Lania, Richard E. Mains, Betty A. Eipper, Constantine A. Stratakis Frontiers in Endocrinology, 2023 IntroductionPituitary adenomas (PAs) are common, usually benign tumors of the anterior pituitary gland which, for the most part, have no known genetic cause. PAs are associated with major clinical effects due to hormonal dysregulation and tumoral impingement on vital brain structures. PAM encodes a multifunctional protein responsible for the essential C-terminal amidation of secreted peptides.MethodsFollowing the identification of a loss-of-function variant (p.Arg703Gln) in the peptidylglycine a-amidating monooxygenase (PAM) gene in a family with pituitary gigantism, we investigated 299 individuals with sporadic PAs and 17 familial isolated PA kindreds for PAM variants. Genetic screening was performed by germline and tumor sequencing and germline copy number variation (CNV) analysis.ResultsIn germline DNA, we detected seven heterozygous, likely pathogenic missense, truncating, and regulatory SNVs. These SNVs were found in sporadic subjects with growth hormone excess (p.Gly552Arg and p.Phe759Ser), pediatric Cushing disease (c.-133T&gt;C and p.His778fs), or different types of PAs (c.-361G&gt;A, p.Ser539Trp, and p.Asp563Gly). The SNVs were functionally tested in vitro for protein expression and trafficking by Western blotting, splicing by minigene assays, and amidation activity in cell lysates and serum samples. These analyses confirmed a deleterious effect on protein expression and/or function. By interrogating 200,000 exomes from the UK Biobank, we confirmed a significant association of the PAM gene and rare PAM SNVs with diagnoses linked to pituitary gland hyperfunction.ConclusionThe identification of PAM as a candidate gene associated with pituitary hypersecretion opens the possibility of developing novel therapeutics based on altering PAM function.
Grainyhead 1 acts as a drug-inducible conserved transcriptional regulator linked to insulin signaling and lifespan Giovanna Grigolon, Elisa Araldi, Reto Erni, Jia Yee Wu, Carolin Thomas, Marco La Fortezza, Beate Laube, Doris Pöhlmann, Markus Stoffel, Kim Zarse, Erick M. Carreira, Michael Ristow, Fabian Fischer Nature Communications, 2022 Aging is impacted by interventions across species, often converging on metabolic pathways. Transcription factors regulate longevity yet approaches for their pharmacological modulation to exert geroprotection remain sparse. We show that increased expression of the transcription factor Grainyhead 1 (GRH-1) promotes lifespan and pathogen resistance in Caenorhabditis elegans. A compound screen identifies FDA-approved drugs able to activate human GRHL1 and promote nematodal GRH-1-dependent longevity. GRHL1 activity is regulated by post-translational lysine methylation and the phosphoinositide (PI) 3-kinase C2A. Consistently, nematodal longevity following impairment of the PI 3-kinase or insulin/IGF-1 receptor requires grh-1. In BXD mice, Grhl1 expression is positively correlated with lifespan and insulin sensitivity. In humans, GRHL1 expression positively correlates with insulin receptor signaling and also with lifespan. Fasting blood glucose levels, including in individuals with type 2 diabetes, are negatively correlated with GRHL1 expression. Thereby, GRH-1/GRHL1 is identified as a pharmacologically malleable transcription factor impacting insulin signaling and lifespan.
Targeted Suppression of miRNA-33 Using pHLIP Improves Atherosclerosis Regression Xinbo Zhang, Noemi Rotllan, Alberto Canfrán-Duque, Jonathan Sun, Jakub Toczek, Anna Moshnikova, Shipra Malik, Nathan L. Price, Elisa Araldi, Wen Zhong, Mehran M. Sadeghi, Oleg A. Andreev, Raman Bahal, Yana K. Reshetnyak, Yajaira Suárez, Carlos Fernández-Hernando Circulation Research, 2022 Background: miRNA therapeutics have gained attention during the past decade. These oligonucleotide treatments can modulate the expression of miRNAs in vivo and could be used to correct the imbalance of gene expression found in human diseases such as obesity, metabolic syndrome, and atherosclerosis. The in vivo efficacy of current anti-miRNA technologies hindered by physiological and cellular barriers to delivery into targeted cells and the nature of miRNAs that allows one to target an entire pathway that may lead to deleterious off-target effects. For these reasons, novel targeted delivery systems to inhibit miRNAs in specific tissues will be important for developing effective therapeutic strategies for numerous diseases including atherosclerosis. Methods: We used pH low-insertion peptide (pHLIP) constructs as vehicles to deliver microRNA-33-5p (miR-33) antisense oligonucleotides to atherosclerotic plaques. Immunohistochemistry and histology analysis was performed to assess the efficacy of miR-33 silencing in atherosclerotic lesions. We also assessed how miR-33 inhibition affects gene expression in monocytes/macrophages by single-cell RNA transcriptomics. Results: The anti-miR-33 conjugated pHLIP constructs are preferentially delivered to atherosclerotic plaque macrophages. The inhibition of miR-33 using pHLIP-directed macrophage targeting improves atherosclerosis regression by increasing collagen content and decreased lipid accumulation within vascular lesions. Single-cell RNA sequencing analysis revealed higher expression of fibrotic genes ( Col2a1, Col3a1, Col1a2, Fn1 , etc) and tissue inhibitor of metalloproteinase 3 ( Timp3 ) and downregulation of Mmp12 in macrophages from atherosclerotic lesions targeted by pHLIP-anti-miR-33. Conclusions: This study provides proof of principle for the application of pHLIP for treating advanced atherosclerosis via pharmacological inhibition of miR-33 in macrophages that avoid the deleterious effects in other metabolic tissues. This may open new therapeutic opportunities for atherosclerosis-associated cardiovascular diseases via selective delivery of other protective miRNAs.
Desmosterol suppresses macrophage inflammasome activation and protects against vascular inflammation and atherosclerosis Xinbo Zhang, Jeffrey G. McDonald, Binod Aryal, Alberto Canfrán‐Duque, Emily L. Goldberg, Elisa Araldi, Wen Ding, Yuhua Fan, Bonne M. Thompson, Abhishek K. Singh, Qian Li, George Tellides, Jose Ordovás-Montanes, Rolando García Milian, Vishwa Deep Dixit, Elina Ikonen, Yajaira Suárez, Carlos Fernández-Hernando Proceedings of the National Academy of Sciences of the United States of America, 2021
Lanosterol Modulates TLR4-Mediated Innate Immune Responses in Macrophages Elisa Araldi, Marta Fernández-Fuertes, Alberto Canfrán-Duque, Wenwen Tang, Gary W. Cline, Julio Madrigal-Matute, Jordan S. Pober, Miguel A. Lasunción, Dianqing Wu, Carlos Fernández-Hernando, Yajaira Suárez Cell Reports, 2017
Chronic miR-29 antagonism promotes favorable plaque remodeling in atherosclerotic mice Victoria Ulrich, Noemi Rotllan, Elisa Araldi, Amelia Luciano, Philipp Skroblin, Mélanie Abonnenc, Paola Perrotta, Xiaoke Yin, Ashley Bauer, Kristen L Leslie, Pei Zhang, Binod Aryal, Rusty L Montgomery, Thomas Thum, Kathleen Martin, Yajaira Suarez, Manuel Mayr, Carlos Fernandez‐Hernando, William C Sessa EMBO Molecular Medicine, 2016
Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis Noemi Rodlan, Aránzazu Chamorro‐Jorganes, Elisa Araldi, Amarylis C. Wanschel, Binod Aryal, Juan F. Aranda, Leigh Goedeke, Alessandro G. Salerno, Cristina M. Ramírez, William C. Sessa, Yajaira Suárez, Carlos Fernández‐Hernando FASEB Journal, 2015
Control of cholesterol metabolism and plasma high-density lipoprotein levels by microRNA-144 Cristina M. Ramírez, Noemi Rotllan, Alexander V. Vlassov, Alberto Dávalos, Mu Li, Leigh Goedeke, Juan F. Aranda, Daniel Cirera-Salinas, Elisa Araldi, Alessandro Salerno, Amarylis Wanschel, Jiri Zavadil, Antonio Castrillo, Jungsu Kim, Yajaira Suárez, Carlos Fernández-Hernando Circulation Research, 2013
Notch pathway activation targets AML-initiating cell homeostasis and differentiation Camille Lobry, Panagiotis Ntziachristos, Delphine Ndiaye-Lobry, Philmo Oh, Luisa Cimmino, Nan Zhu, Elisa Araldi, Wenhuo Hu, Jacquelyn Freund, Omar Abdel-Wahab, Sherif Ibrahim, Dimitris Skokos, Scott A. Armstrong, Ross L. Levine, Christopher Y. Park, Iannis Aifantis Journal of Experimental Medicine, 2013
A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia Apostolos Klinakis, Camille Lobry, Omar Abdel-Wahab, Philmo Oh, Hiroshi Haeno, Silvia Buonamici, Inge van De Walle, Severine Cathelin, Thomas Trimarchi, Elisa Araldi, Cynthia Liu, Sherif Ibrahim, Miroslav Beran, Jiri Zavadil, Argiris Efstratiadis, Tom Taghon, Franziska Michor, Ross L. Levine, Iannis Aifantis Nature, 2011
Type 2 diabetes risk alleles in peptidyl-glycine alpha-amidating monooxygenase influence GLP-1 levels and response to GLP-1 receptor agonists MM Umapathysivam, E Araldi, B Hastoy, AY Dawed, H Vatandaslar, ... Genome Medicine , 2026 2026 Citations: 11
Effect of Empagliflozin on the plasma lipidome in patients with type 2 diabetes mellitus: results from the EmDia clinical trial KI Bauer, D Baker, R Lerner, T Koeck, G Buch, Z Fischer, R Martens, ... Cardiovascular Diabetology 24 (1), 359 , 2025 2025 Citations: 6
Unraveling the link between cholesterol and immune system in cancer: From biological mechanistic insights to clinical evidence. A narrative review F Pecci, V Cognigni, GC Giudice, F Paoloni, L Cantini, KS Saini, ... Critical Reviews in Oncology/Hematology 209, 104654 , 2025 2025 Citations: 7
Autophagy regulator ATG7 links lipid metabolism to cell-fate decisions in kidney tubule health and disease D Nieri, SA Keller, L Pierre, F Carloni, R Pili, Z Chen, AM Ouellette, ... medRxiv, 2025.03. 26.25324675 , 2025 2025 Citations: 1
A map of the lipid–metabolite–protein network to aid multi-omics integration UA Anyaegbunam, AC Vagiona, V Ten Cate, K Bauer, T Schmidlin, ... Biomolecules 15 (4), 484 , 2025 2025 Citations: 3
Unbiased multi-omics network-based data integration allows clinically relevant outcome-predicting clustering of individuals with heart failure EE Esenkova, T Koeck, R Lerner, D Baker, KI Bauer, M Nuber, G Valentini, ... medRxiv, 2025.01. 28.25321241 , 2025 2025
Individuals with heart failure stratified by their left ventricular ejection fraction display distinct lipidomic signatures: insights from the MyoVasc study M Olkowicz, R Lerner, A Gieswinkel, Z Fischer, V Ten Cate, E Araldi, ... 2025
Retraction of: Lithium treatment extends human lifespan: findings from the UK Biobank E Araldi, CR Jutzeler, M Ristow Aging (Albany NY) 16 (17), 12431 , 2024 2024
Sec24D-positive ER exit sites sort raftpreferring proteins for rapid ER export I Castello-Serrano, R Ippolito, K Levental, E Araldi, I Levental FEBS OPEN BIO 14, 74-74 , 2024 2024
Effect of Empagliflozin compared to placebo on the plasma lipidome in patients with type 2 diabetes mellitus-results from the EmDia trial K Bauer, D Baker, R Lerner, Z Fischer, T Koeck, G Buch, E Esenkova, ... FEBS OPEN BIO 14, 159-159 , 2024 2024
Type 2 diabetes risk alleles in peptidyl-glycine alpha-amidating monooxygenase influence GLP-1 levels and response to GLP-1 receptor agonists E Araldi, MM Umapathysivam, B Hastoy, AY Dawed, H Vatandaslar, ... FEBS OPEN BIO 14, 467-467 , 2024 2024
Unbiased clustering and molecular characterisation of novel metabolic phenotypes in a heart failure cohort E Esenkova, T Koeck, G Valentini, P Wild, E Casiraghi, E Araldi Cardiovascular Research 120 (Supplement_1), cvae088. 087 , 2024 2024
A systematic review of lipid-focused cardiovascular disease research: trends and opportunities UA Anyaegbunam, P More, JF Fontaine, V Cate, K Bauer, U Distler, ... Current Issues in Molecular Biology 45 (12), 9904-9916 , 2023 2023 Citations: 9
Germline loss-of-function PAM variants are enriched in subjects with pituitary hypersecretion G Trivellin, AF Daly, LC Hernández-Ramírez, E Araldi, C Tatsi, RK Dale, ... Frontiers in Endocrinology 14, 1166076 , 2023 2023 Citations: 22
Effects of antidiabetic drugs on mortality risks in individuals with type 2 diabetes: A prospective cohort study of UK Biobank participants E Araldi, CR Jutzeler, M Ristow medRxiv, 2023.05. 19.23290214 , 2023 2023 Citations: 4
Lithium treatment extends human lifespan: findings from the UK Biobank E Araldi, CR Jutzeler, M Ristow Aging (Albany NY) 15 (2), 421 , 2023 2023 Citations: 22
Targeted suppression of miRNA-33 using pHLIP improves atherosclerosis regression X Zhang, N Rotllan, A Canfrán-Duque, J Sun, J Toczek, A Moshnikova, ... Circulation Research 131 (1), 77-90 , 2022 2022 Citations: 86
Grainyhead 1 acts as a drug-inducible conserved transcriptional regulator linked to insulin signaling and lifespan G Grigolon, E Araldi, R Erni, JY Wu, C Thomas, M La Fortezza, B Laube, ... Nature communications 13 (1), 107 , 2022 2022 Citations: 21
Desmosterol suppresses macrophage inflammasome activation and protects against vascular inflammation and atherosclerosis X Zhang, JG McDonald, B Aryal, A Canfrán‐Duque, EL Goldberg, E Araldi, ... Proceedings of the National Academy of Sciences 118 (47), e2107682118 , 2021 2021 Citations: 130
Targeted suppression of microRNA-33 in lesional macrophages using pH low-insertion peptides (pHLIP) improves atherosclerotic plaque regression X Zhang, N Rotllan, A Canfrán-Duque, J Toczek, A Moshnikova, S Malik, ... 2020 Citations: 1
MOST CITED SCHOLAR PUBLICATIONS
A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia A Klinakis, C Lobry, O Abdel-Wahab, P Oh, H Haeno, S Buonamici, ... Nature 473 (7346), 230-233 , 2011 2011 Citations: 454
The HIF signaling pathway in osteoblasts directly modulates erythropoiesis through the production of EPO EB Rankin, C Wu, R Khatri, TLS Wilson, R Andersen, E Araldi, AL Rankin, ... Cell 149 (1), 63-74 , 2012 2012 Citations: 363
MicroRNA-148a regulates LDL receptor and ABCA1 expression to control circulating lipoprotein levels L Goedeke, N Rotllan, A Canfrán-Duque, JF Aranda, CM Ramírez, ... Nature medicine 21 (11), 1280-1289 , 2015 2015 Citations: 310
MicroRNA-16 and microRNA-424 regulate cell-autonomous angiogenic functions in endothelial cells via targeting vascular endothelial growth factor receptor-2 and fibroblast … A Chamorro-Jorganes, E Araldi, LOF Penalva, D Sandhu, ... Arteriosclerosis, thrombosis, and vascular biology 31 (11), 2595-2606 , 2011 2011 Citations: 306
Control of cholesterol metabolism and plasma high-density lipoprotein levels by microRNA-144 CM Ramírez, N Rotllan, AV Vlassov, A Dávalos, M Li, L Goedeke, ... Circulation research 112 (12), 1592-1601 , 2013 2013 Citations: 270
Macrophage deficiency of miR‐21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis A Canfrán‐Duque, N Rotllan, X Zhang, M Fernández‐Fuertes, ... EMBO molecular medicine 9 (9), 1244-1262 , 2017 2017 Citations: 235
Notch pathway activation targets AML-initiating cell homeostasis and differentiation C Lobry, P Ntziachristos, D Ndiaye-Lobry, P Oh, L Cimmino, N Zhu, ... Journal of Experimental Medicine 210 (2), 301-319 , 2013 2013 Citations: 201
Hypoxia, HIFs and bone development E Araldi, E Schipani Bone 47 (2), 190-196 , 2010 2010 Citations: 194
MicroRNAs as pharmacological targets in endothelial cell function and dysfunction A Chamorro-Jorganes, E Araldi, Y Suárez Pharmacological research 75, 15-27 , 2013 2013 Citations: 141
MiR-155 has a protective role in the development of non-alcoholic hepatosteatosis in mice AM Miller, DS Gilchrist, J Nijjar, E Araldi, CM Ramirez, CA Lavery, ... PloS one 8 (8), e72324 , 2013 2013 Citations: 140
Desmosterol suppresses macrophage inflammasome activation and protects against vascular inflammation and atherosclerosis X Zhang, JG McDonald, B Aryal, A Canfrán‐Duque, EL Goldberg, E Araldi, ... Proceedings of the National Academy of Sciences 118 (47), e2107682118 , 2021 2021 Citations: 130
VEGF‐independent cell‐autonomous functions of HIF‐1α regulating oxygen consumption in fetal cartilage are critical for chondrocyte survival C Maes, E Araldi, K Haigh, R Khatri, R Van Looveren, AJ Giaccia, ... Journal of Bone and Mineral Research 27 (3), 596-609 , 2012 2012 Citations: 125
Lanosterol modulates TLR4-mediated innate immune responses in macrophages E Araldi, M Fernández-Fuertes, A Canfrán-Duque, W Tang, GW Cline, ... Cell reports 19 (13), 2743-2755 , 2017 2017 Citations: 123
Genetic ablation of miR-33 increases food intake, enhances adipose tissue expansion, and promotes obesity and insulin resistance NL Price, AK Singh, N Rotllan, L Goedeke, A Wing, A Canfrán-Duque, ... Cell reports 22 (8), 2133-2145 , 2018 2018 Citations: 120
ANGPTL4 deficiency in haematopoietic cells promotes monocyte expansion and atherosclerosis progression B Aryal, N Rotllan, E Araldi, CM Ramírez, S He, BG Chousterman, ... Nature communications 7 (1), 12313 , 2016 2016 Citations: 118
MicroRNA-140 and the silencing of osteoarthritis E Araldi, E Schipani Genes & development 24 (11), 1075-1080 , 2010 2010 Citations: 104
miR-27b inhibits LDLR and ABCA1 expression but does not influence plasma and hepatic lipid levels in mice L Goedeke, N Rotllan, CM Ramírez, JF Aranda, A Canfrán-Duque, ... Atherosclerosis 243 (2), 499-509 , 2015 2015 Citations: 89
Targeted suppression of miRNA-33 using pHLIP improves atherosclerosis regression X Zhang, N Rotllan, A Canfrán-Duque, J Sun, J Toczek, A Moshnikova, ... Circulation Research 131 (1), 77-90 , 2022 2022 Citations: 86
Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice V Ulrich, N Rotllan, E Araldi, A Luciano, P Skroblin, M Abonnenc, ... EMBO molecular medicine 8 (6), 643-653 , 2016 2016 Citations: 86
Improved repair of dermal wounds in mice lacking micro RNA‐155 C van Solingen, E Araldi, A Chamorro‐Jorganes, C Fernández‐Hernando, ... Journal of cellular and molecular medicine 18 (6), 1104-1112 , 2014 2014 Citations: 82
