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1. Human blood vessel organoids reveal a critical role for CTGF in maintaining microvascular integrity

Author

Romeo, Sara G., Secco, Ilaria, Schneider, Edoardo, Reumiller, Christina M., Santos, Celio X. C., Zoccarato, Anna, Musale, Vishal, Pooni, Aman, Yin, Xiaoke, Theofilatos, Konstantinos, Trevelin, Silvia Cellone, Zeng, Lingfang, Mann, Giovanni E., Pathak, Varun, Harkin, Kevin, Stitt, Alan W., Medina, Reinhold J., Margariti, Andriana, Mayr, Manuel, Shah, Ajay M., Giacca, Mauro, and Zampetaki, Anna

Published
2023
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3. Unveiling impaired vascular function and cellular heterogeneity in diabetic donor-derived vascular organoids

Author

Naderi-Meshkin, Hojjat, Wahyu Setyaningsih, Wiwit A, Yacoub, Andrew, Carney, Garrett, Cornelius, Victoria A, Nelson, Clare-Ann, Kelaini, Sophia, Donaghy, Clare, Dunne, Philip D, Amirkhah, Raheleh, Zampetaki, Anna, Zeng, Lingfang, Stitt, Alan W, Lois, Noemi, Grieve, David J, and Margariti, Andriana

Abstract

Vascular organoids (VOs), derived from induced pluripotent stem cells (iPSCs), hold promise as in vitro disease models and drug screening platforms. However, their ability to faithfully recapitulate human vascular disease and cellular composition remains unclear. In this study, we demonstrate that VOs derived from iPSCs of donors with diabetes (DB-VOs) exhibit impaired vascular function compared to non-diabetic VOs (ND-VOs). DB-VOs display elevated levels of reactive oxygen species (ROS), heightened mitochondrial content and activity, increased proinflammatory cytokines, and reduced blood perfusion recovery in vivo. Through comprehensive single-cell RNA sequencing, we uncover molecular and functional differences, as well as signaling networks, between vascular cell types and clusters within DB-VOs. Our analysis identifies major vascular cell types (endothelial cells [ECs], pericytes, and vascular smooth muscle cells) within VOs, highlighting the dichotomy between ECs and mural cells. We also demonstrate the potential need for additional inductions using organ-specific differentiation factors to promote organ-specific identity in VOs. Furthermore, we observe basal heterogeneity within VOs and significant differences between DB-VOs and ND-VOs. Notably, we identify a subpopulation of ECs specific to DB-VOs, showing overrepresentation in the ROS pathway and underrepresentation in the angiogenesis hallmark, indicating signs of aberrant angiogenesis in diabetes. Our findings underscore the potential of VOs for modeling diabetic vasculopathy, emphasize the importance of investigating cellular heterogeneity within VOs for disease modeling and drug discovery, and provide evidence of GAP43 (neuromodulin) expression in ECs, particularly in DB-VOs, with implications for vascular development and disease.Graphical Abstract

Published
2024
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5. BS16 Blood vessel organoids derived from diabetic patients revealed impaired function based on a subpopulation of endothelial cells

Author

Naderi-Meshkin, Hojjat, primary, Eleftheriadou, Magdalini, additional, Carney, Garrett, additional, Cornelius, Victoria A, additional, Nelson, Clare-Ann, additional, Kelaini, Sophia, additional, Yacoub, Andrew, additional, Dunne, Philip D, additional, Amirkhah, Raheleh, additional, Zampetaki, Anna, additional, Zeng, Lingfang, additional, Stitt, Alan W, additional, Lois, Naomi, additional, Grieve, David J, additional, and Margariti, Andriana, additional

Published
2023
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7. Targeting QKI-7 in vivo restores endothelial cell function in diabetes

Author

Yang, Chunbo, Eleftheriadou, Magdalini, Kelaini, Sophia, Morrison, Thomas, González, Marta Vilà, Caines, Rachel, Edwards, Nicola, Yacoub, Andrew, Edgar, Kevin, Moez, Arya, Ivetic, Aleksandar, Zampetaki, Anna, Zeng, Lingfang, Wilkinson, Fiona L., Lois, Noemi, Stitt, Alan W., Grieve, David J., and Margariti, Andriana

Published
2020
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9. Oral Presentation No. 093 Assessing different noncoding RNAs as markers of platelet reactivity

Author

Gutmann, Clemens, primary, Barwari, Temo, additional, Schulte, Christian, additional, Singh, Bhawana, additional, Theofilatos, Konstantinos, additional, Joshi, Abhishek, additional, Zampetaki, Anna, additional, Chan, Melissa V, additional, Armstrong, Paul C, additional, Kiechl, Stefan, additional, Willeit, Johann, additional, Warner, Timothy D, additional, and Mayr, Manuel, additional

Published
2022
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10. Human blood vessel organoids reveal a critical role for CTGF in maintaining microvascular integrity

Author

Romeo, Sara G, primary, Secco, Ilaria, additional, Schneider, Edoardo, additional, Reumiller, Christina M, additional, Santos, Celio XC, additional, Pooni, Aman, additional, Yin, Xiaoke, additional, Theofilatos, Konstantinos, additional, Trevelin, Silvia Cellone, additional, Zeng, Lingfang, additional, Mann, Giovanni E, additional, Margariti, Andriana, additional, Mayr, Manuel, additional, Shah, Ajay M, additional, Giacca, Mauro, additional, and Zampetaki, Anna, additional

Published
2022
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11. Impaired Function in Diabetic Patient iPSCs-derived Blood Vessel Organoids Stem from a Subpopulation of Vascular Cells

Author

Naderi-Meshkin, Hojjat, primary, Eleftheriadou, Magdalini, additional, Carney, Garrett, additional, Cornelius, Victoria A, additional, Nelson, Clare-Ann, additional, Kelaini, Sophia, additional, Yacoub, Andrew, additional, Donaghy, Clare, additional, Dunne, Philip D, additional, Amirkhah, Raheleh, additional, Zampetaki, Anna, additional, Zeng, Lingfang, additional, Stitt, Alan W, additional, Grieve, David J, additional, and Margariti, Andriana, additional

Published
2022
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19. Glycoproteomics Reveals Decorin Peptides With Anti-Myostatin Activity in Human Atrial Fibrillation

Author

Barallobre-Barreiro, Javier, Gupta, Shashi K., Zoccarato, Anna, Kitazume-Taneike, Rika, Fava, Marika, Yin, Xiaoke, Werner, Tessa, Hirt, Marc N., Zampetaki, Anna, Viviano, Alessandro, Chong, Mei, Bern, Marshall, Kourliouros, Antonios, Domenech, Nieves, Willeit, Peter, Shah, Ajay M., Jahangiri, Marjan, Schaefer, Liliana, Fischer, Jens W., Iozzo, Renato V., Viner, Rosa, Thum, Thomas, Heineke, Joerg, Kichler, Antoine, Otsu, Kinya, and Mayr, Manuel

Published
2016
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20. Nox2-deficient Tregs improve heart transplant outcomes via their increased graft recruitment and enhanced potency

Author

Trevelin, Silvia C., primary, Zampetaki, Anna, additional, Sawyer, Greta, additional, Ivetic, Aleksandar, additional, Brewer, Alison C., additional, Smyth, Lesley Ann, additional, Marelli-Berg, Federica, additional, Köchl, Robert, additional, Lechler, Robert I., additional, Shah, Ajay M., additional, and Lombardi, Giovanna, additional

Published
2021
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21. Signature of circulating microRNAs in osteoarthritis

Author

Beyer, Christian, Zampetaki, Anna, Lin, Neng-Yu, Kleyer, Arnd, Perricone, Carlo, Iagnocco, Annamaria, Distler, Alfiya, Langley, Sarah R, Gelse, Kolja, Sesselmann, Stefan, Lorenzini, Rolando, Niemeier, Andreas, Swoboda, Bernd, Distler, Jörg HW, Santer, Peter, Egger, Georg, Willeit, Johann, Mayr, Manuel, Schett, Georg, and Kiechl, Stefan

Published
2015
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23. Lacking cytokine production in ES cells and ES-cell-derived vascular cells stimulated by TNF-[alpha] is rescued by HDAC inhibitor trichostatin A

Author

Zampetaki, Anna, Zeng, Lingfang, Xiao, Qingzhong, Margariti, Andriani, Hu, Yanhua, and Xu, Qingbo

Subjects
Tumor necrosis factor -- Influence, Tumor necrosis factor -- Properties, Embryonic stem cells -- Properties, Cell physiology -- Research, Biological sciences
Abstract

Inflammation and TNF-[alpha] signaling play a central role in most of the pathological conditions where cell transplantation could be applied. As shown by initial experiments, embryonic stem (ES) cells and ES-cell derived vascular cells express very low levels of TNF-[alpha] receptor I (TNFRp55) and thus do not induce cytokine expression in response to TNF-[alpha] stimulation. Transient transfection analysis of wild-type or deletion variants of the TNFRp55 gene promoter showed a strong activity for a 250-bp fragment in the upstream region of the gene. This activity was abolished by mutations targeting the Spl/Sp3 or AP1 binding sites. Moreover, treatment with trichostatin A (TSA) led to a pronounced increase in TNFRp55 mRNA and promoter activity. Overexpression of Spl or c-fos further enhanced the TSA-induced luciferase activity, and this response was attenuated by Sp3 or c-jun coexpression. Additional experiments revealed that TSA did not affect the Spl/Sp3 ratio but caused transcriptional activation of the c-fos gene. Thus, we provide the first evidence that ES and ES-cell-derived vascular cells lack cytokine expression in response to TNF-[alpha] stimulation due to low levels of c-fos and transcriptional activation of Spl that can be regulated by inhibition of histone deacetylase activity. inflammation; TNFRp55; c-fos; Spl

Published
2007

24. HDAC3 is crucial in shear- and VEGF-induced stem cell differentiation toward endothelial cells

Author

Zeng, Lingfang, Xiao, Qingzhong, Margariti, Andriana, Zhang, Zhongyi, Zampetaki, Anna, Patel, Seema, Capogrossi, Maurizio C., Hu, Yanhua, and Xu, Qingbo

Subjects
Stem cells -- Analysis, Cell differentiation -- Analysis, Vascular endothelial growth factor -- Analysis, Biological sciences
Abstract

Reendothelialization involves endothelial progenitor cell (EPC) homing, proliferation, and differentiation, which may be influenced by fluid shear stress and local flow pattern. This study aims to elucidate the role of laminar flow on embryonic stem (ES) cell differentiation and the underlying mechanism. We demonstrated that laminar flow enhanced ES cell-derived progenitor cell proliferation and differentiation into endothelial cells (ECs). Laminar flow stabilized and activated histone deacetylase 3 (HDAC3) through the Flk-1-Pl3K-Akt pathway, which in turn deacetylated p53, leading to p21 activation. A similar signal pathway was detected in vascular endothelial growth factor-induced EC differentiation. HDAC3 and p21 were detected in blood vessels during embryogenesis. Local transfer of ES cell-derived EPC incorporated into injured femoral artery and reduced neointima formation in a mouse model. These data suggest that shear stress is a key regulator for stem cell differentiation into EC, especially in EPC differentiation, which can be used for vascular repair, and that the Flk-1-Pl3K-Akt-HDAC3-p53-p21 pathway is crucial in such a process.

Published
2006

25. Biomechanical stress induces IL-6 expression in smooth muscle cells via Ras/Rac1-p38 MAPK-NF-[kappa]B signaling pathways

Author

Zampetaki, Anna, Zhang, Zhongyi, Hu, Yanhua, and Xu, Qingbo

Subjects
Interleukin-6 -- Research, Interleukin-6 -- Physiological aspects, Cytokines -- Research, Cytokines -- Physiological aspects, Stress (Physiology) -- Research, Smooth muscle -- Research, Smooth muscle -- Physiological aspects, Biological sciences
Abstract

IL-6, a proinflammatory cytokine, has been implicated in the development of vascular diseases. We previously demonstrated that mechanical stress can initiate signaling pathways leading to smooth muscle cell (SMC) proliferation and apoptosis, but little is known concerning cyclic stress-induced inflammatory response. To explore the role of stretch in the upregulation of cytokine expression in SMCs we performed RNase protection assay for a panel of cytokines and found that mechanical stress resulted in a time-dependent induction of IL 6 mRNA but not other cytokines, e.g., IL-1[alpha], IL-1[beta], IL-6, IL-10, IL-12p35, IL- 12p40, IL- 18, IFN-[gamma], and macrophage migration inhibitory factor (MIF). This induction also correlated with elevated IL-6 protein levels in the supernatant. Pretreatment of the cells with NF-[kappa]B inhibitors inhibited NF-[kappa]B activity and resulted in marked inhibition (50%) of IL-6 protein. Moreover, SMC lines stably expressing dominant-negative Ras (RasN17) or Rac (RacN17) exhibited a remarkable decrease in p38 MAPK activity and IL-6 mRNA induction by mechanical stress. Furthermore, a significant inhibition of 30 and 40% in IL-6 protein was observed in SMCs pretreated with inhibitors of p38 MAPK and ERK1/2, respectively, but not JNK. Interestingly, SMCs isolated from PKC-[delta]-deficient mice exhibited higher levels of IL-6 compared with wild-type cells. Finally, high levels of IL-6 expression were observed in atherosclerotic lesions of vein bypass grafts, which are related to altered biomechanical stress. Our findings demonstrate that biomechanical stress-induced IL-6 expression occurs via a mechanism that involves Ras/Rac/p38 MAPK/NF-[kappa]B/NF-IL6 signaling pathways, which is downregulated by PKC-[delta], and suggest that modulation of this event contributes to the pathogenesis of atherosclerosis. mechanical stress; interleukin-6; signal transduction; atherosclerosis

Published
2005

26. Metabolic recovery after weight loss surgery is reflected in serum microRNAs

Author

Sangiao-Alvarellos, Susana, primary, Theofilatos, Konstantinos, additional, Barwari, Temo, additional, Gutmann, Clemens, additional, Takov, Kaloyan, additional, Singh, Bhawana, additional, Juiz-Valiña, Paula, additional, Varela-Rodríguez, Bárbara María, additional, Outeiriño-Blanco, Elena, additional, Duregotti, Elisa, additional, Zampetaki, Anna, additional, Lunger, Lukas, additional, Ebenbichler, Christoph, additional, Tilg, Herbert, additional, García-Brao, María Jesús, additional, Willeit, Peter, additional, Mena, Enrique, additional, Kiechl, Stefan, additional, Cordido, Fernando, additional, and Mayr, Manuel, additional

Published
2020
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33. 'Young at heart': Regenerative potential linked to immature cardiac phenotypes

Author

Gomes, Renata S.M., Skroblin, Philipp, Munster, Alex B., Tomlins, Hannah, Langley, Sarah R., Zampetaki, Anna, Yin, Xiaoke, Wardle, Fiona C., and Mayr, Manuel

Subjects
Proteomics, animal structures, Proteome, Short Communication, Heart Ventricles, Muscle Proteins, Cardiomyocyte, Myofilament, Mice, Animals, Humans, Regeneration, Myocytes, Cardiac, Molecular Biology, Zebrafish, Stem cell, LC-MS/MS, liquid chromatography tandem mass spectrometry, Microfilament Proteins, Troponin I, fungi, DIGE, difference in-gel electrophoresis, Gene Expression Regulation, Developmental, Heart, MicroRNAs, MI, myocardial infarction, Transcriptome, Cardiology and Cardiovascular Medicine
Abstract

The adult human myocardium is incapable of regeneration; yet, the zebrafish (Danio rerio) can regenerate damaged myocardium. Similar to the zebrafish heart, hearts of neonatal, but not adult mice are capable of myocardial regeneration. We performed a proteomics analysis of adult zebrafish hearts and compared their protein expression profile to hearts from neonatal and adult mice. Using difference in-gel electrophoresis (DIGE), there was little overlap between the proteome from adult mouse (> 8 weeks old) and adult zebrafish (18 months old) hearts. Similarly, there was a significant degree of mismatch between the protein expression in neonatal and adult mouse hearts. Enrichment analysis of the selected proteins revealed over-expression of DNA synthesis-related proteins in the cardiac proteome of the adult zebrafish heart similar to neonatal and 4 days old mice, whereas in hearts of adult mice there was a mitochondria-related predominance in protein expression. Importantly, we noted pronounced differences in the myofilament composition: the adult zebrafish heart lacks many of the myofilament proteins of differentiated adult cardiomyocytes such as the ventricular isoforms of myosin light chains and nebulette. Instead, troponin I and myozenin 1 were expressed as skeletal isoforms rather than cardiac isoforms. The relative immaturity of the adult zebrafish heart was further supported by cardiac microRNA data. Our assessment of zebrafish and mammalian hearts challenges the assertions on the translational potential of cardiac regeneration in the zebrafish model. The immature myofilament composition of the fish heart may explain why adult mouse and human cardiomyocytes lack this endogenous repair mechanism., Graphical abstract, Highlights • Proteomics reveals minimal overlap between adult mouse and adult zebrafish hearts. • Gene expression analysis confirms profound differences in myofilament composition. • The adult zebrafish heart is more similar to a newborn mouse heart. • The relative immaturity is further supported by cardiac microRNA data.

Published
2016
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34. Long-Noncoding RNA Structure and Function:Is there a link?

Author

Zampetaki, Anna, Albrecht, Andreas, and Steinhofel, Kathleen Kristine

Subjects
Noncoding RNA, lncRNA, RNA structure, gene editing, cardiovascular diseases
Abstract

RNA has emerged as the prime target for diagnostics, therapeutics and the development of personalized medicine. In particular, the noncoding RNAs (ncRNAs) that do not encode proteins, display remarkable biochemical versatility. They can fold into complex structures and interact with proteins, DNA and other RNAs, modulating the activity, DNA targets or partners of multiprotein complexes. Thus, ncRNAs confer regulatory plasticity and represent a new layer of epigenetic control that is dysregulated in disease. Intriguingly, for long noncoding RNAs (lncRNAs, >200 nucleotides length) structural conservation rather than nucleotide sequence conservation seems to be crucial for maintaining their function. LncRNAs tend to acquire complex secondary and tertiary structures and their functions only impose very subtle sequence constraints. In the present review we will discuss the biochemical assays that can be employed to determine the lncRNA structural configurations. The implications and challenges of linking function and lncRNA structure to design novel RNA therapeutic approaches will also be analyzed.

Published
2018

36. Enhanced Function of Induced Pluripotent Stem Cell-Derived Endothelial Cells Through ESM1 Signaling

Author

Vilà-González, Marta, primary, Kelaini, Sophia, additional, Magee, Corey, additional, Caines, Rachel, additional, Campbell, David, additional, Eleftheriadou, Magdalini, additional, Cochrane, Amy, additional, Drehmer, Daiana, additional, Tsifaki, Marianna, additional, O'Neill, Karla, additional, Pedrini, Edoardo, additional, Yang, Chunbo, additional, Medina, Reinhold, additional, McDonald, Denise, additional, Simpson, David, additional, Zampetaki, Anna, additional, Zeng, Lingfang, additional, Grieve, David, additional, Lois, Noemi, additional, Stitt, Alan W., additional, and Margariti, Andriana, additional

Published
2018
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37. Inhibition of profibrotic microRNA-21 affects platelets and their releasate

Author

Barwari, Temo, primary, Eminaga, Seda, additional, Mayr, Ursula, additional, Lu, Ruifang, additional, Armstrong, Paul C., additional, Chan, Melissa V., additional, Sahraei, Mahnaz, additional, Fernández-Fuertes, Marta, additional, Moreau, Thomas, additional, Barallobre-Barreiro, Javier, additional, Lynch, Marc, additional, Yin, Xiaoke, additional, Schulte, Christian, additional, Baig, Ferheen, additional, Pechlaner, Raimund, additional, Langley, Sarah R., additional, Zampetaki, Anna, additional, Santer, Peter, additional, Weger, Martin, additional, Plasenzotti, Roberto, additional, Schosserer, Markus, additional, Grillari, Johannes, additional, Kiechl, Stefan, additional, Willeit, Johann, additional, Shah, Ajay M., additional, Ghevaert, Cedric, additional, Warner, Timothy D., additional, Fernández-Hernando, Carlos, additional, Suárez, Yajaira, additional, and Mayr, Manuel, additional

Published
2018
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39. Crispr/Cas9 gene editing reveals novel tertiary constraints in clustered mirna processing

Author

Lataniotis, Lazaros, Albrecht, Andreas A., Kok, Fatma, Monfries, Clinton, Benedetti, Lorena, Lawson, Nathan D., Hughes, Simon M., Steinhofel, Kathleen, Mayr, Manuel, and Zampetaki, Anna

Abstract

MicroRNAs (miRNAs) play an important role in the cellular function. They often form families, with members sharing high sequence homology, a property that hampers miRNA research as there is a lack of elegant tools for specific miRNA manipulation.

Published
2017

41. Abstract 300: MicroRNA-21 Affects Platelets and Their Releasate: A Novel Mechanism for the Anti-Fibrotic Effects of MicroRNA-21 Inhibition

Author

Barwari, Temo, primary, Eminaga, Seda, additional, Lu, Ruifang, additional, Armstrong, Paul C, additional, Schulte, Christian, additional, Lynch, Marc, additional, Chan, Melissa V, additional, Barallobre-Barreiro, Javier, additional, Yin, Xiaoke, additional, Pechlaner, Raimund, additional, Langley, Sarah, additional, Sahraei, Mahnaz, additional, Fernández-Fuertes, Marta, additional, Zampetaki, Anna, additional, Santer, Peter, additional, Warner, Timothy D, additional, Kiechl, Stefan, additional, Willeit, Johann, additional, Fernández-Hernando, Carlos, additional, Suárez, Yajaira, additional, Shah, Ajay M, additional, and Mayr, Manuel, additional

Published
2018
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42. 82 Microrna-21 regulates transforming growth factor beta-1 release from platelets

Author

Barwari, Temo, primary, Eminaga, Seda, additional, Armstrong, Paul, additional, Chan, Melissa, additional, Lu, Ruifang, additional, Barallobre-Barreiro, Javier, additional, Yin, Xiaoke, additional, Pechlaner, Raimund, additional, Langley, Sarah, additional, Zampetaki, Anna, additional, Santer, Peter, additional, Weger, Martin, additional, Warner, Timothy, additional, Kiechl, Stefan, additional, Willeit, Johann, additional, Shah, Ajay, additional, and Mayr, Manuel, additional

Published
2018
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45. Guidelines for the functional annotation of microRNAs using the Gene Ontology

Author

Huntley, Rachael P., Sitnikov, Dmitry, Orlic-Milacic, Marija, Balakrishnan, Rama, D'Eustachio, Peter, Gillespie, Marc E., Howe, Doug, Kalea, Anastasia Z., Maegdefessel, Lars, Osumi-Sutherland, David, Petri, Victoria, Smith, Jennifer R., Van Auken, Kimberly, Wood, Valerie, Zampetaki, Anna, Mayr, Manuel, Lovering, Ruth C., Huntley, Rachael P [0000-0001-6718-3559], Sitnikov, Dmitry [0000-0002-5283-5283], Orlic-Milacic, Marija [0000-0002-3218-5631], Balakrishnan, Rama [0000-0003-2468-9933], Gillespie, Marc E [0000-0002-5766-1702], Howe, Doug [0000-0001-5831-7439], Kalea, Anastasia Z [0000-0001-5775-3984], Maegdefessel, Lars [0000-0001-5228-2634], Osumi-Sutherland, David [0000-0002-7073-9172], Petri, Victoria [0000-0002-5540-8498], Van Auken, Kimberly [0000-0002-1706-4196], Wood, Valerie [0000-0001-6330-7526], Mayr, Manuel [0000-0002-0597-829X], Lovering, Ruth C [0000-0002-9791-0064], and Apollo - University of Cambridge Repository

Subjects
function, microRNA, analysis, biocuration, Annotation, Guidelines as Topic, MicroRNA, Biocuration, Mice, MicroRNAs, annotation, GO, Animals, Humans, Gene Silencing, Function, Analysis
Abstract

MicroRNA regulation of developmental and cellular processes is a relatively new field of study, and the available research data have not been organized to enable its inclusion in pathway and network analysis tools. The association of gene products with terms from the Gene Ontology is an effective method to analyze functional data, but until recently there has been no substantial effort dedicated to applying Gene Ontology terms to microRNAs. Consequently, when performing functional analysis of microRNA data sets, researchers have had to rely instead on the functional annotations associated with the genes encoding microRNA targets. In consultation with experts in the field of microRNA research, we have created comprehensive recommendations for the Gene Ontology curation of microRNAs. This curation manual will enable provision of a high-quality, reliable set of functional annotations for the advancement of microRNA research. Here we describe the key aspects of the work, including development of the Gene Ontology to represent this data, standards for describing the data, and guidelines to support curators making these annotations. The full microRNA curation guidelines are available on the GO Consortium wiki (http://wiki.geneontology.org/index.php/MicroRNA-GO-annotation-manual).

Published
2016

50. Circulating MicroRNA-122 Is Associated With the Risk of New-Onset Metabolic Syndrome and Type 2 Diabetes

Author

Willeit, Peter, primary, Skroblin, Philipp, additional, Moschen, Alexander R., additional, Yin, Xiaoke, additional, Kaudewitz, Dorothee, additional, Zampetaki, Anna, additional, Barwari, Temo, additional, Whitehead, Meredith, additional, Ramírez, Cristina M., additional, Goedeke, Leigh, additional, Rotllan, Noemi, additional, Bonora, Enzo, additional, Hughes, Alun D., additional, Santer, Peter, additional, Fernández-Hernando, Carlos, additional, Tilg, Herbert, additional, Willeit, Johann, additional, Kiechl, Stefan, additional, and Mayr, Manuel, additional

Published
2016
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