Staff member


Jonel Trebicka

Visiting Researcher
Integrative Cell and Tissue Dynamics
jtrebicka@ibecbarcelona.eu
+34 934 037 068
Staff member publications

Beiert, T., Knappe, V., Tiyerili, V., Stöckigt, F., Effelsberg, V., Linhart, M., Steinmetz, M., Klein, S., Schierwagen, R., Trebicka, J., Roell, W., Nickenig, G., Schrickel, J. W., Andrié, R. P., (2018). Chronic lower-dose relaxin administration protects from arrhythmia in experimental myocardial infarction due to anti-inflammatory and anti-fibrotic properties International Journal of Cardiology 250, 21-28

Background: The peptide hormone relaxin-2 (RLX) exerts beneficial effects during myocardial ischemia, but functional data on lower-dose RLX in myocardial infarction (MI) is lacking. Therefore, we investigated the impact of 75 

Keywords: Arrhythmia, Myocardial infarction, Relaxin-2, Ventricular tachycardia


Trebicka, J., Gluud, L. L., (2017). Reply to: “Adding embolization to TIPS implantation: A better therapy to control bleeding from ectopic varices?” Journal of Hepatology 67, (1), 202-203

We would like to thank the Perricone and colleagues for their letter and for the interest in the article “Emergency TIPS in a Child-Pugh B patient: When does the window of opportunity open and close?”.1 The letter raises an important question, namely the management of bleeding from ectopic varices. Bleeding from ectopic varices other than fundic varices represents a rare and challenging complication. Guidance for clinical practice is needed.


Jansen, C., Thiele, M., Verlinden, W., Krag, A., Francque, S., Trebicka, J., (2017). Prediction of presence of oesophageal varices just by shear-wave elastography of the liver and spleen Liver International 37, (9), 1406-1407

Reiberger, T., Trebicka, J., (2017). New liver – Fresh microbiome: Implications on brain function Liver Transplantation 23, (7), 873-874

Schierwagen, R., Uschner, F. E., Magdaleno, F., Klein, S., Trebicka, J., (2017). Rationale for the use of statins in liver disease American Journal of Physiology - Gastrointestinal and Liver Physiology 312, (5), G407-G412

The evolution of chronic liver injuries from benign and manageable dysfunction to life threatening end-stage liver disease with severe complications renders chronic liver disease a global health burden. Because of the lack of effective medication, transplantation remains the only and final curative option for end-stage liver disease. Since the demand for organ transplants by far exceeds the supply, other treatment options are urgently required to prevent progression and improve end-stage liver disease. Statins are primarily cholesterol-lowering drugs used for primary or secondary prevention of cardiovascular diseases. In addition to the primary effect, statins act beneficially through different pleiotropic mechanisms on inflammation, fibrosis, endothelial function, thrombosis, and coagulation to improve chronic liver diseases. However, concerns remain about the efficacy and safety of statin treatment because of their potential hepatotoxic risks, and as of now, these risks impede broader use of statins in the treatment of chronic liver diseases. The aim of this review is to comprehensively describe the mechanisms by which statins improve prospects for different chronic liver diseases with special focus on the pathophysiological rationale and the clinical experience of statin use in the treatment of liver diseases.


Beiert, T., Tiyerili, V., Knappe, V., Effelsberg, V., Linhart, M., Stöckigt, F., Klein, S., Schierwagen, R., Trebicka, J., Nickenig, G., Schrickel, J. W., Andrié, R. P., (2017). Relaxin reduces susceptibility to post-infarct atrial fibrillation in mice due to anti-fibrotic and anti-inflammatory properties Biochemical and Biophysical Research Communications 490, (3), 643-649

Background Relaxin-2 (RLX) is a peptide hormone that exerts beneficial anti-fibrotic and anti-inflammatory effects in diverse models of cardiovascular disease. The goal of this study was to determine the effects of RLX treatment on the susceptibility to atrial fibrillation (AF) after myocardial infarction (MI). Methods Mice with cryoinfarction of the left anterior ventricular wall were treated for two weeks with either RLX (75

Keywords: Atrial fibrillation, Atrial fibrosis, Myocardial infarction, Relaxin-2


Schwab, S., Lehmann, J., Lutz, P., Jansen, C., Appenrodt, B., Lammert, F., Strassburg, C. P., Spengler, U., Nischalke, H. D., Trebicka, J., (2017). Influence of genetic variations in the SOD1 gene on the development of ascites and spontaneous bacterial peritonitis in decompensated liver cirrhosis European Journal of Gastroenterology and Hepatology 29, (7), 800-804

Background The balance between generation and elimination of reactive oxygen species by superoxide dismutase (SOD) is crucially involved in the pathophysiology of liver cirrhosis. Reactive oxygen species damage cells and induce inflammation/fibrosis, but also play a critical role in immune defense from pathogens. As both processes are involved in the development of liver cirrhosis and its complications, genetic variation of the SOD1 gene was investigated. Patients and methods Two SOD1 single nucleotide polymorphisms (rs1041740 and rs3844942) were analyzed in 49 cirrhotic patients undergoing liver transplantation. In addition, 344 cirrhotic patients with ascites were analyzed in a cohort of 521 individuals in terms of the relationship of these polymorphisms with spontaneous bacterial peritonitis (SBP). Results Although rs3844942 showed no associations with complications of cirrhosis, we observed a significant association between rs1041740 and the presence of ascites and SBP in the discovery cohort of patients with cirrhosis. Importantly, the association with SBP was not confirmed in the validation cohort of patients with ascites. By contrast, a trend toward lower SBP rates was observed in carriers of rs1041740. In this cohort, rs1041740 was not associated with survival. Conclusion These data suggest a complex role of SOD1 in different processes leading to complications of liver cirrhosis. rs1041740 might be associated with the development of ascites and possibly plays a role in SBP once ascites has developed.

Keywords: Ascites, Genetic polymorphism, Liver cirrhosis, Reactive oxygen stress, Spontaneous bacterial peritonitis, Superoxide dismutases


Klein, S., Schierwagen, R., Uschner, F. E., Trebicka, J., (2017). Mouse and rat models of induction of hepatic fibrosis and assessment of portal hypertension Fibrosis (Methods in Molecular Biology) (ed. Rittié, L.), Humana Press (New York, USA) 1627, 91-116

Portal hypertension either develops due to progressive liver fibrosis or is the consequence of vascular liver diseases such as portal vein thrombosis or non-cirrhotic portal hypertension. This chapter focuses on different rodent models of liver fibrosis with portal hypertension and also in few non-cirrhotic portal hypertension models. Importantly, after the development of portal hypertension, the proper assessment of drug effects in the portal and systemic circulation should be discussed. The last part of the chapter is dedicated in these techniques to assess the in vivo hemodynamics and the ex vivo techniques of the isolated liver perfusion and vascular contractility.

Keywords: Aortic ring contraction, Bile duct ligation, Carbon tetrachloride, Colored microsphere technique, High-fat diet, Isolated in situ liver perfusion, Methionine-choline-deficient diet, Partial portal vein ligation, Portal hypertension