Prof. Dr. med. Natascha Sommer, PhD

Professorship “Mitochondrial Signaling in Pulmonary Vascular and Airway Diseases”

Natascha Sommer focuses on the transfer of fundamental, preclinical scientific concepts to clinical practice, as well as the implementation of clinical questions into experimental problem solutions ("from bench to bedside and from bedside to bench"). This has been achieved by setting up a basic scientific working group in the field of pulmonary vascular and airway remodeling with a focus on mechanisms dependent on mitochondria and reactive oxygen species. In parallel, clinical work guarantees close contact to patients and other clinicians for optimal translational research and conduct of clinical trials.

Prof. Dr. med., Natascha Sommer, PhD
Justus Liebig University Giessen
Professorship for Mitochondrial Signaling in Pulmonary Vascular and Airway Diseases
Head of the Outpatient Clinic for Pneumology

Specific research areas:

  • Acute oxygen sensing and signaling mechanisms
  • Reactive oxygen species (ROS)-related mechanisms in COPD
  • Mitochondrial signaling in hypoxia-induced PH, emphysema and inflammation
  • Clinical trials in COPD and human immune cell sampling

Specific methodology:

  1. Mitochondrial methods
    Respirometry (also in combination with fluorescence measurements), ROS detection using fluorescent dyes/protein-based probes/electron spin resonance spectroscopy, redox measurements using remission spectrophotometry, determination of mitochondrial morphology and calcium regulation by confocal microscopy and 3D live cell imaging, biochemical methods (Blue Native Gels and Complexome analyses)
  2. Disease modeling
    Tobacco smoke-induced pulmonary hypertension, monocrotaline-induced pulmonary hypertension, murine smoke-induced pulmonary emphysema and hypertension, double-hit model of smoke-induced emphysema and virus infection, hyperoxia-induced pulmonary damage, LPS-induced acute lung injury, ex vivo isolated ventilated and perfused mouse lung
  3. Clinical studies/samples
    Human material (serum, peripheral blood mononuclear cells, bronchoalveolar lavage (BAL), biopsies, and cultured lung sections) from patients with chronic obstructive pulmonary disease and pulmonary hypertension