
Dr. Philipp Hohensinner
Department of Medicine II (Division of Cardiology)
Position: Research Associate (Postdoc)
ORCID: 0000-0003-4819-3190
T +43 1 40400 73515
philipp.hohensinner@meduniwien.ac.at
Keywords
Aging, Premature; Atherosclerosis; Macrophages; Monocytes
Research interests
My current main research interest is to define cellular changes within an atherosclerotic plaque.
Techniques, methods & infrastructure
- In vitro cell culture,
- animal models,
- qPCR,
- flow cytometry,
- molecular biology techniques
Selected publications
- Hohensinner, P.J. et al., 2018. Reduction of Premature Aging Markers After Gastric Bypass Surgery in Morbidly Obese Patients.
- Hohensinner, P.J. et al., 2017. PAI-1 (Plasminogen Activator Inhibitor-1) Expression Renders Alternatively Activated Human Macrophages Proteolytically Quiescent.
- Hohensinner, P.J. et al., 2016. Age intrinsic loss of telomere protection via TRF1 reduction in endothelial cells. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1863(2), pp.360-367. Available at: http://dx.doi.org/10.1016/j.bbamcr.2015.11.034.
- Li, Y. et al., 2016. Deficient Activity of the Nuclease MRE11A Induces T Cell Aging and Promotes Arthritogenic Effector Functions in Patients with Rheumatoid Arthritis. Immunity, 45(4), pp.903-916. Available at: http://dx.doi.org/10.1016/j.immuni.2016.09.013.
- Hohensinner, P.J., Goronzy, J.J. & Weyand, C.M., 2014. Targets of Immune Regeneration in Rheumatoid Arthritis. Mayo Clinic Proceedings, 89(4), pp.563-575. Available at: http://dx.doi.org/10.1016/j.mayocp.2014.01.020.