PhD student in cardiac biology (m/w/d)

Starting as soon as possible at the Internal Medicine for the Department of Cardiology, Angiology, and Pneumology.

The innovative research project focuses on developing and translating a novel peptide therapy against cardiac diseases. It is based on extensive preliminary work by our team, demonstrating therapeutic effects of the synthetic peptide in chronic and acute heart failure animal models.

The therapeutic peptide is derived from the protein S100A1, which is central to maintaining normal heart function. The synthetic peptide (S100A1ct) mimics the native protein's function in the heart muscle and, because of its pharmacokinetic and pharmacodynamic properties, can be developed as a candidate for experimental therapy of myocardial insufficiency.

The project aims to develop additional cell-permeable S100A1ct peptidomimetics with extended therapeutic capabilities and investigate their cardioprotective effects in models such as anthracycline-induced cardiotoxicity (AICT) and heart failure with preserved/reduced ejection fraction.

References:

• Kehr D, Ritterhoff J, Glaser M, Jarosch L, Salazar R, Spaich K, Varadi K, Birkenstock J, Egger M, Gao E, Koch WJ, Katus HA, Frey N, Jungmann A, Busch CJ, Mather PJ, Ruhparwar A, Voelkers M, Wade RC, Most P: S100A1ct: a synthetic peptide derived from human S100A1 protein improves cardiac contractile performance and survival in pre-clinical heart failure models. 2024 Nov 21. doi: 10.1161/CIRCULATIONAHA.123.066961. Online ahead of print.
• Volkers M, Loughrey CM, Macquaide N, Remppis A, DeGeorge BR, Jr., Wegner FV, Friedrich O, Fink RH, Koch WJ, Smith GL, and Most P (2007) S100A1 decreases calcium spark frequency and alters their spatial characteristics in permeabilized adult ventricular cardiomyocytes. Cell Calcium 41: 135-143 doi: 10.1016/j.ceca.2006.06.001
• Most P, Remppis A, Weber C, Bernotat J, Ehlermann P, Pleger ST, Kirsch W, Weber M, Uttenweiler D, Smith GL, Katus HA, and Fink RH (2003) The C terminus (amino acids 75-94) and the linker region (amino acids 42-54) of the Ca2+-binding protein S100A1 differentially enhance sarcoplasmic Ca2+ release in murine skinned skeletal muscle fibers. J Biol Chem 278: 26356-26364 doi: 10.1074/jbc.M303338200

Your Tasks

• Responsible planning and implementation of experiments within the scientific project plan
• Develop and establish new laboratory methods for research approaches
• Isolation of primary cardiomyocytes and analysis of contractility and calcium transients
• Establishment of in vivo disease models to test therapeutic efficacy of S100A1ct and other peptides
• Interaction with collaboration partners and core facilities, supporting other scientists
• Participation in scientific events with contributions

Your Profile

• Completed university degree in natural sciences (biology, molecular medicine, cardiovascular sciences)
• Knowledge of standard methodologies in molecular and cellular biology (primary cell culture, qPCR, WB, histology)
• Experience in cardiovascular research methods (cardiomyocyte isolation, in vitro contractility analysis, small animal models, echocardiography) is advantageous
• Excellent English skills (written and oral), basic German knowledge
• Strong analytical thinking, teamwork, self-organization, and responsibility

About us

For further information, contact Tamara Kantzos via email.

Interested?

Applications are accepted until 18.05.2025 online.