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Detail

Philipp Hohensinner
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

  1. Hohensinner, P.J. et al., 2018. Reduction of Premature Aging Markers After Gastric Bypass Surgery in Morbidly Obese Patients.
  2. Hohensinner, P.J. et al., 2017. PAI-1 (Plasminogen Activator Inhibitor-1) Expression Renders Alternatively Activated Human Macrophages Proteolytically Quiescent.
  3. 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.
  4. 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.
  5. 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.