Diversity of myofibroblast phenotypes in heart failure

The postdoc position is embedded in the broader project on cardiac fibrosis and the underlying mechanisms, a core research topic in Experimental Cardiology. We have previously established the diversity of myofibroblasts in the heart after myocardial infarction (Nagaraju et al., 2017) and their interaction with cardiac myocytes (Nagaraju, Dries et al., 2019). We have also reported the reversibility of the myofibroblast phenotype in the human heart in late stages of heart failure (Nagaraju et al., 2019). Presently we address diversity of fibrosis and myofibroblast cell types in different disease etiologies through gene-expression studies, asking which cell profiles regulate unwanted fibrosis and hold promise of reversibility. Rich transcriptomics data are the starting point for functional mechanistic studies exploring phenotype diversity and impact on cardiac function, in particular interactions with cardiac myocytes. The postdoctoral fellow will lead these functional studies using live cell imaging and assessing membrane transport and electrophysiology, with manipulation of signaling pathways and gene expression.  

External funding supports the position and the research. The Department of Cardiovascular Sciences has extensive facilities for functional confocal imaging, electrophysiology and molecular studies. Human fibroblastic cells and cells from ischemic cardiomyopathy are available in a continuous program and biobanking further supports access to tissue and cells.

Selected references

Nagaraju CK, et al. Myofibroblast Phenotype and Reversibility of Fibrosis in Patients With End-Stage Heart Failure. J Am Coll Cardiol. 2019 May 14;73(18):2267-2282.doi: 10.1016/j.jacc.2019.02.049.

Nagaraju CK, Dries E, et al. 2019. Myofibroblast modulation of cardiac myocyte structure and function. Sci Rep, 2019; 9(1):8879. doi: 10.1038/s41598-019-45078-2.

Nagaraju CK, et al. Global fibroblast activation throughout the left ventricle but localized fibrosis after myocardial infarction. Sci Rep. 2017 Sep 7;7(1):10801. doi:10.1038/s41598-017-09790-1.