Joerg Heineke
Professor at Heidelberg University
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About
Professor Joerg Heineke is a faculty member at Heidelberg University in Germany. His research primarily focuses on diabetic cardiomyopathy and the modulation of the cardiomyocyte stress response. Recent articles authored by Professor Heineke explore the protective roles of C1q and Tumor Necrosis Factor Related Protein 9 in alleviating cardiac insulin resistance and inflammation, as well as the regulatory impact of endothelial cell GATA2 on long non-coding RNAs.
Positions (1)
Joerg Heineke
Heidelberg University
3 months ago
The PhD project "Interorgan Interaction in Cardiometabolic Heart Failure" at Heidelberg University offers an exciting opportunity to investigate the molecular mechanisms underlying heart failure, with a particular focus on interorgan crosstalk in models of heart failure with preserved ejection fraction (HFpEF). The research will be conducted in the group of Professor Joerg Heineke at the Medical Faculty Mannheim, Heidelberg University, renowned for its excellent research facilities and dynamic academic environment. The project builds on preliminary findings that identified a secreted factor capable of protecting against diastolic heart dysfunction and suppressing obesity. The successful candidate will explore these molecular mechanisms further and assess potential therapeutic options using genetic mouse models. The research will employ a wide range of technologies, including genetics, imaging, biochemistry, molecular biology, cell culture, experimental animal work, and both bulk and single cell next-generation sequencing (NGS) approaches. Applicants should possess a Master’s degree or equivalent in biological sciences or a related discipline, with a strong foundation in molecular and cell biology. Experience in cardiac and/or metabolism biology, bioinformatics, and disease modelling (including a FELASA certificate) is highly desirable. Good English language skills are required to succeed in this international research environment. The position is full-time and based at the European Center for Angioscience, Department of Cardiovascular Physiology, Medical Faculty Heidelberg, located in Mannheim, Germany. The project is not funded by the EU Research Framework Programme. The application deadline is 30 June 2026, and the anticipated start date is 1 September 2026. To apply, candidates must submit their application exclusively through the HBIGS application system. For further information about the research group and project details, visit the Department of Cardiovascular Physiology website. For questions, contact HBIGS at [email protected]. This PhD project is ideal for motivated students interested in advanced cardiovascular research, molecular biology, and translational medicine. It offers the opportunity to work in a collaborative and innovative academic setting, contributing to the understanding and treatment of cardiometabolic heart failure.
3 months ago
Articles (3)
Fibrosis is a hallmark of chronic disease. Although fibroblasts are involved, it is unclear to what extent endothelial cells also might contribute. We detected increased expression of the transcription factor Sox9 in endothelial cells in several different mouse fibrosis models. These models included systolic heart failure induced by pressure overload, diastolic heart failure induced by high-fat diet and nitric oxide synthase inhibition, pulmonary fibrosis induced by bleomycin treatment, and liver fibrosis due to a choline-deficient diet. We also observed up-regulation of endothelial SOX9 in cardiac tissue from patients with heart failure. To test whether SOX9 induction was sufficient to cause disease, we generated mice with endothelial cell–specific overexpression of Sox9 , which promoted fibrosis in multiple organs and resulted in signs of heart failure. Endothelial Sox9 deletion prevented fibrosis and organ dysfunction in the two mouse models of heart failure as well as in the lung and liver fibrosis mouse models. Bulk and single-cell RNA sequencing of mouse endothelial cells across multiple vascular beds revealed that SOX9 induced extracellular matrix, growth factor, and inflammatory gene expression, leading to matrix deposition by endothelial cells. Moreover, mouse endothelial cells activated neighboring fibroblasts that then migrated and deposited matrix in response to SOX9, a process partly mediated by the secreted growth factor CCN2, a direct SOX9 target; endothelial cell–specific Sox9 deletion reversed these changes. These findings suggest a role for endothelial SOX9 as a fibrosis-promoting factor in different mouse organs during disease and imply that endothelial cells are an important regulator of fibrosis.
Year:
2024
Year:
2023
Year:
2022
Collaborators (4)
Gergana Dobreva
Heidelberg University
Felix A. Trogisch
Ruprecht-Karls-Universität Heidelberg Medizinische Fakultät Mannheim
Ralf Kist
Senior Lecturer in Oral Biology
Newcastle University
Oliver J. Müller
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