Bernhard J. Haubner

ORCID: 0000-0003-1766-8720
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About
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Research Areas
  • Congenital heart defects research
  • Cardiac Fibrosis and Remodeling
  • Cardiac Structural Anomalies and Repair
  • Tissue Engineering and Regenerative Medicine
  • Cardiac Ischemia and Reperfusion
  • Cardiac Imaging and Diagnostics
  • Adipose Tissue and Metabolism
  • Cardiovascular Function and Risk Factors
  • Congenital Heart Disease Studies
  • Nitric Oxide and Endothelin Effects
  • Pancreatic function and diabetes
  • Autophagy in Disease and Therapy
  • Cardiomyopathy and Myosin Studies
  • Advanced MRI Techniques and Applications
  • Signaling Pathways in Disease
  • High Altitude and Hypoxia
  • Travel-related health issues
  • Apelin-related biomedical research
  • Cardiac Arrest and Resuscitation
  • Parathyroid Disorders and Treatments
  • Genomics and Chromatin Dynamics
  • Adenosine and Purinergic Signaling
  • Diabetes Treatment and Management
  • Ion Channels and Receptors
  • Intensive Care Unit Cognitive Disorders

Innsbruck Medical University
2009-2024

Austrian Academy of Sciences
2012-2024

Institute of Molecular Biotechnology
2012-2024

University Hospital of Zurich
2020-2024

University of Zurich
2021-2024

Universität Innsbruck
2015-2019

Lung Institute
2018

Imperial College London
2018

Institute of Genetics and Cancer
2018

University of Edinburgh
2018

Background: Heart failure (HF) survival has improved, and nowadays, many patients with HF die of noncardiac causes, including cancer. Our aim was to investigate whether a causal relationship exists between the development Methods: induced by inflicting large anterior myocardial infarction in APC min mice, which are prone developing precancerous intestinal tumors, tumor growth measured. In addition, rule out hemodynamic impairment, heterotopic heart transplantation model used an infarcted or...

10.1161/circulationaha.117.030816 article EN Circulation 2018-02-19

Rationale : Cardiac remodeling and subsequent heart failure remain critical issues after myocardial infarction despite improved treatment reperfusion strategies. Recently, cardiac regeneration has been demonstrated in fish newborn mice apex resection or infarctions. Two key to translate findings model organisms future therapies humans: what is the mechanism can indeed occur humans? Objective To assess whether human neonatal hearts functionally recover infarction. Methods Results Here, we...

10.1161/circresaha.115.307017 article EN Circulation Research 2015-12-10

Cardiac remodeling and subsequent heart failure remain critical issues after myocardial infarction despite improved treatment reperfusion strategies. Recently, complete cardiac regeneration has been demonstrated in fish newborn mice following resection of the apex. However, it remained entirely unclear whether mammalian can also completely regenerate a complex ischemic injury. We established protocol to induce severe attack one-day-old using left anterior descending artery (LAD) ligation....

10.18632/aging.100526 article EN cc-by Aging 2012-12-31

The growth factor neuregulin stimulates heart muscle repair in newborn mice and from human infants if given during a specific therapeutic time period.

10.1126/scitranslmed.aaa5171 article EN Science Translational Medicine 2015-04-01

Article24 June 2019Open Access Source DataTransparent process Apelin inhibition prevents resistance and metastasis associated with anti-angiogenic therapy Iris Uribesalgo Corresponding Author [email protected] orcid.org/0000-0001-9492-1000 Institute of Molecular Biotechnology the Austrian Academy Sciences (IMBA), Vienna BioCenter, Vienna, Austria Search for more papers by this author David Hoffmann Yin Zhang Department Microbiology, Tumor Cell Biology, Biomedicum, Karolinska Institutet,...

10.15252/emmm.201809266 article EN cc-by EMBO Molecular Medicine 2019-06-24

Abstract Aims Newborn mice and humans display transient cardiac regenerative potential that rapidly declines postnatally. Patients who survive a myocardial infarction (MI) often develop chronic heart failure due to the heart’s poor regeneration capacity. We hypothesized ‘regenerative-to-scarring’ transition might be driven by perinatal shifts observed in circulating T-cell compartment. Methods results Post-MI immune responses were characterized 1- (P1) vs. 7-day-old (P7) subjected left...

10.1093/eurheartj/ehac153 article EN cc-by-nc European Heart Journal 2022-03-11

Objective Endothelial dysfunction by the loss of nitric oxide (NO) is a critical event during reperfusion ischemic myocardium. Reduced NO availability signals important pathophysiological changes leading to myocardial injury. We have recently shown that biosynthesis can be disturbed endogenous synthase (NOS) inhibitor ADMA and these are mediated an impairment its metabolism dimethylarginine dimethylaminohydrolase (DDAH). therefore analyzed role in setting ischemia reperfusion.

10.1016/j.cardiores.2007.04.030 article EN Cardiovascular Research 2007-05-06

Cardiac regeneration is one of the prime visions in cardiovascular research. The mouse neonatal apical resection and left anterior descending artery (LAD) ligation model introduced novel vivo mammalian assays to study cardiac regeneration. However, recent reports editorials discussed critically questioned value technical reproducibility myocardial infarction approach, making it paramount develop use a reproducible system. We established by visually confirmed LAD using microsurgery....

10.1007/s00395-016-0580-3 article EN cc-by Basic Research in Cardiology 2016-09-24

Lamina-associated polypeptide (LAP)2alpha is a mammalian chromatin-binding protein that interacts with fraction of A-type lamins in the nuclear interior. Because mutations and LAP2alpha lead to cardiac disorders humans, we hypothesized these factors may play important roles heart development adult tissue homeostasis.We asked whether presence was required for normal function.To study molecular mechanisms disease, analyzed structure function complete conditional Lap2alpha(-/-) mice as well...

10.1161/circresaha.109.205724 article EN Circulation Research 2009-11-20

Background PI3Kγ functions in the immune compartment to promote inflammation response G-protein-coupled receptor (GPCR) agonists and also acts within heart itself both as a negative regulator of cardiac contractility pro-survival factor. Thus, has potential limit M I/R injury. Methodology/Principal Findings Complete PI3Kγ−/− mutant mice, catalytically inactive PI3KγKD/KD (KD) knock-in control wild type (WT) mice were subjected vivo myocardial ischemia reperfusion (M I/R) Additionally,...

10.1371/journal.pone.0009350 article EN cc-by PLoS ONE 2010-02-19

The ability to perceive noxious stimuli is critical for an animal's survival in the face of environmental danger, and thus pain perception likely be under stringent evolutionary pressure. Using a neuronal-specific RNAi knock-down strategy adult Drosophila, we recently completed genome-wide functional annotation heat nociception that allowed us identify α2δ3 as novel gene. Here report construction evolutionary-conserved, system-level, global molecular network map. Our systems map markedly...

10.1371/journal.pgen.1003071 article EN cc-by PLoS Genetics 2012-12-06

Abstract Sodium glucose transporter (SGLT)-2 inhibitors have consistently shown cardioprotective effects independent of the glycemic status treated patients. In this study we aimed to investigate underlying mechanisms short-term empagliflozin treatment in a mouse model type II diabetes. Male db/db mice were fed western diet with or without enrichment for 7 days. While tolerance was significantly improved mice, body weight and fasting insulin levels comparable both groups. Cardiac signaling...

10.1038/s41598-020-76698-8 article EN cc-by Scientific Reports 2020-11-12

Background: The adult mammalian heart has little regenerative capacity after myocardial infarction (MI), whereas neonatal mouse regenerates without scarring or dysfunction. However, the underlying pathways are poorly defined. We sought to derive insights into regulating development of and cardiac regeneration post-MI. Methods Results: Total RNA-seq through first 10 days postnatal life (referred as P3, P5, P10) revealed a previously unobserved transition in microRNA (miRNA) expression between...

10.1161/circgen.117.001805 article EN Circulation Genomic and Precision Medicine 2018-02-01

Abstract Klotho is an antiaging protein which exerts known cardioprotection. In kidney, trans-membrane acts as essential co-receptor of fibroblast growth factor 23 (FGF23). the heart, soluble (sKlotho) protects from systolic dysfunction independently FGF23. Here, we analyzed association FGF23 and sKlotho upon progression chronic heart failure (CHF) expression in human hearts. Serum levels were measured 287 patients with cardiomyopathy (CMP). Tissue samples CMP (n = 10) healthy control hearts...

10.1038/s41598-018-26539-6 article EN cc-by Scientific Reports 2018-05-24

To perform cardiac imaging in mice without having to invest expensive dedicated equipment, we adapted a clinical 1.5 Tesla (T) magnetic resonance (MRI) scanner for use murine ischemia/reperfusion model. Phase‐sensitive inversion recovery (PSIR) sequence facilitated the determination of infarct sizes vivo by late gadolinium enhancement. Results were compared histological areas after procedure with good correlation ( r = 0.807, P < .001). In addition, fractional area change (FAC) was...

10.1155/2011/185683 article EN cc-by BioMed Research International 2010-12-05

Aim: Although the risk factors for delirium in general medicine are well-established, their significance cardiac diseases remains to be determined. Therefore, we evaluated predisposing and precipitating patients hospitalized with acute chronic heart disease. Methods Results: In this observational cohort study, 1,042 elderly (≥65 years) admitted cardiology wards, 167 875 without delirium, were included. The relevant sociodemographic cardiac- medical-related clusters assessed by simple...

10.3389/fcvm.2021.686665 article EN cc-by Frontiers in Cardiovascular Medicine 2021-09-29

AimsIncreased myocardial wall strain triggers the cardiac hypertrophic response by increasing cardiomyocyte size, reprogramming gene expression, and enhancing contractile protein synthesis. The LIM protein, migfilin, is a cytoskeleton-associated that was found to translocate in vitro into nucleus Ca2+-dependent manner, where it co-activates pivotal transcription factor Csx/Nkx2.5. However, vivo role of migfilin function stress unclear.

10.1093/cvr/cvv125 article EN Cardiovascular Research 2015-04-07
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