Thomas Thum

ORCID: 0000-0003-4360-1511
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About
Contact & Profiles
Research Areas
  • MicroRNA in disease regulation
  • Circular RNAs in diseases
  • Cancer-related molecular mechanisms research
  • Cardiac Fibrosis and Remodeling
  • Extracellular vesicles in disease
  • Cardiovascular Function and Risk Factors
  • RNA modifications and cancer
  • RNA Interference and Gene Delivery
  • Cardiomyopathy and Myosin Studies
  • Nitric Oxide and Endothelin Effects
  • RNA Research and Splicing
  • Tissue Engineering and Regenerative Medicine
  • Heart Failure Treatment and Management
  • Viral Infections and Immunology Research
  • Cardiac Structural Anomalies and Repair
  • Angiogenesis and VEGF in Cancer
  • Signaling Pathways in Disease
  • Cardiac Ischemia and Reperfusion
  • Transplantation: Methods and Outcomes
  • Cardiac Valve Diseases and Treatments
  • CRISPR and Genetic Engineering
  • Cardiovascular Disease and Adiposity
  • Congenital heart defects research
  • Pharmacogenetics and Drug Metabolism
  • Fuel Cells and Related Materials

Medizinische Hochschule Hannover
2016-2025

Fraunhofer Institute for Toxicology and Experimental Medicine
2003-2024

Translational Therapeutics (United States)
2011-2024

Brescia University
2024

Fraunhofer Research Institution for Materials Recycling and Resource Strategies IWKS
2023-2024

Hannover Re (Germany)
2023

German Centre for Cardiovascular Research
2013-2022

Medical University of Vienna
2022

Imperial College London
2011-2021

Hammersmith Hospital
2008-2021

In response to stress, the heart undergoes extensive cardiac remodeling that results in fibrosis and pathological growth of cardiomyocytes (hypertrophy), which contribute failure. Alterations microRNA (miRNA) levels are associated with dysfunctional gene expression profiles many cardiovascular disease conditions; however, miRNAs have emerged recently as paracrine signaling mediators. Thus, we investigated a potential miRNA crosstalk between fibroblasts found secrete miRNA-enriched exosomes....

10.1172/jci70577 article EN Journal of Clinical Investigation 2014-04-16

Background— Chronic heart failure is characterized by left ventricular remodeling and reactivation of a fetal gene program; the underlying mechanisms are only partly understood. Here we provide evidence that cardiac microRNAs, recently discovered key regulators expression, contribute to transcriptional changes observed in failure. Methods Results— Cardiac transcriptome analyses revealed striking similarities between failing human tissue. Using microRNA arrays, profound alterations expression...

10.1161/circulationaha.107.687947 article EN Circulation 2007-07-03

Long noncoding RNAs represent a novel class of molecules regulating gene expression. are present in body fluids, but their potential as biomarkers was never investigated cardiovascular disease.To study the role long heart disease.Global transcriptomic analyses were done plasma RNA from patients with or without left ventricular remodeling after myocardial infarction. Regulated candidates validated 3 independent patient cohorts developing cardiac and failure (788 patients). The mitochondrial...

10.1161/circresaha.114.303915 article EN Circulation Research 2014-03-25

Pathological growth of cardiomyocytes (hypertrophy) is a major determinant for the development heart failure, one leading medical causes mortality worldwide. Here we show that microRNA (miRNA)-212/132 family regulates cardiac hypertrophy and autophagy in cardiomyocytes. Hypertrophic stimuli upregulate cardiomyocyte expression miR-212 miR-132, which are both necessary sufficient to drive hypertrophic MiR-212/132 null mice protected from pressure-overload-induced whereas cardiomyocyte-specific...

10.1038/ncomms2090 article EN cc-by-nc-sa Nature Communications 2012-09-25

Abstract —Asymmetrical dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor. It formed by protein arginine N -methyltransferases (PRMTs), which utilize S -adenosylmethionine as methyl group donor. ADMA plasma concentration elevated in hypercholesterolemia, leading to endothelial dysfunction and producing proatherogenic changes of cell function. Four different isoforms human PRMTs have been identified. Because the release from cells increased presence native or oxidized...

10.1161/01.res.87.2.99 article EN Circulation Research 2000-07-21

Uncoupling of the endothelial nitric oxide synthase (eNOS) resulting in superoxide anion (O(2)(-)) formation instead (NO) causes diabetic dysfunction. eNOS regulates mobilization and function progenitor cells (EPCs), key regulators vascular repair. We postulate a role uncoupling for reduced number EPC diabetes. levels patients were significantly compared with those control subjects. EPCs from produced excessive O(2)(-) showed impaired migratory capacity nondiabetic NOS inhibition...

10.2337/db06-0699 article EN Diabetes 2007-02-27

Background— Myocardial infarction leads to cardiac remodeling and development of heart failure. Insufficient myocardial capillary density after has been identified as a critical event in this process, although the underlying mechanisms angiogenesis are mechanistically not well understood. Methods Results— Here, we show that small noncoding RNA microRNA-24 (miR-24) is enriched endothelial cells considerably upregulated ischemia. MiR-24 induces cell apoptosis, abolishes network formation on...

10.1161/circulationaha.111.039008 article EN Circulation 2011-07-26

Recent studies highlighted long noncoding RNAs (lncRNAs) to play an important role in cardiac development. However, understanding of lncRNAs diseases is still limited. Global lncRNA expression profiling indicated that several transcripts are deregulated during pressure overload-induced hypertrophy mice. Using stringent selection criteria, we identified Chast (cardiac hypertrophy-associated transcript) as a potential candidate influences cardiomyocyte hypertrophy. Cell fractionation...

10.1126/scitranslmed.aaf1475 article EN Science Translational Medicine 2016-02-17

Cardiac fibroblasts (CFs) drive extracellular matrix remodeling after pressure overload, leading to fibrosis and diastolic dysfunction. Recent studies described the role of long noncoding RNAs (lncRNAs) in cardiac pathologies. Nevertheless, detailed reports on lncRNAs regulating CF biology describing their implication are still missing.Here, we aimed at characterizing lncRNA expression murine CFs chronic overload identify CF-enriched investigate function contribution dysfunction.Global...

10.1161/circresaha.117.310624 article EN Circulation Research 2017-06-20

Cardiac microRNA-132-3p (miR-132) levels are increased in patients with heart failure (HF) and mechanistically drive cardiac remodelling processes. CDR132L, a specific antisense oligonucleotide, is first-in-class miR-132 inhibitor that attenuates even reverses HF preclinical models. The aim of the current clinical Phase 1b study was to assess safety, pharmacokinetics, target engagement, exploratory pharmacodynamic effects CDR132L on standard-of-care therapy for chronic ischaemic randomized,...

10.1093/eurheartj/ehaa898 article EN cc-by-nc European Heart Journal 2020-10-16
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