Heart failure with preserved ejection fraction (HFpEF) is commonly associated with systemic inflammation. It has been posited that disruption of immune homeostasis underlies functional and structural remodeling of the microvessels, thereby leading to diastolic dysfunctionality of the myocardium. Intervention on this pathogenic pathway is anticipated to serve as the much-needed therapeutic strategy against HFpEF. However, cellular and molecular mechanism underlying the crosstalk between the immune and cardiovascular system in HFpEF pathogenesis is yet to be uncovered. Here we set off to investigate the entwined immune-vascular-cardiac interactions. Our goal is not only to shed more light into the mechanistic insights, but also to identify potential therapeutic candidates capable of preventing adverse cardiovascular remodeling. To this end, we focus on elucidating the role of the gut and microbial metabolites in the regulation of the multi-systemic crosstalk by exploiting optical translucency and genetic tractability of the zebrafish as a disease model.

We use a range of techniques in zebrafish genetics, molecular biology, advanced microscopy, and transcriptomic analysis.

For more information and for applying follow this link:
https://www.mdc-berlin.de/career/jobs/phd-student

Scheduled maintenance in progress.