Organ failure is a common consequence of trauma-induced shock and inflammation. In the intensive care unit, failure of vital organs is one of the most frequent causes of death. Organ failure arises for example due to tissue damage after inflammatory reactions or due to insufficient oxygen supply that is caused as a result of circulation disturbances and shock.
The group of Andrey Kozlov researches the underlying molecular mechanisms of trauma-, shock- and inflammation-induced organ failure. The focus is put on the dysfunction of different subcellular structures such as mitochondria, the endoplasmatic reticulum or the nucleus. Furthermore, pathological intracellular signaling cascades are examined that rely for example on gaseous messengers (nitric oxides, carbon monoxide, hydrogen sulphide) or intracellular redox reactions. Other research focuses on:
- Impact of mitochondrial reactive oxygen species (ROS) on systemic inflammatory response syndrome (SIRS)- or sepsis-induced organ failure
- Nitric oxide (NO)-mediated mechanisms of neuronal dysfunction induced through traumatic brain injuries
- Impact of stress on the endoplasmic reticulum during the development of shock- or sepsis-induced organ failure
- Pathophysiological role of free reactive iron species in hypoxic tissues during the development of organ failure
- Reactive oxygen species (ROS)-mediated lung injury in acute respiratory distress syndrome (ARDS) and Corona virus disease 2019 (COVID-19)
- Mitochondria and reactive oxygen species-mediated mechanisms of stem cell activation
- Pathophysiological role of STAT- and AIF-mediated processes during the development of inflammation reactions and cancer
The aim is to develop new diagnostic methods that facilitate the treatment of organ failure. Focus is put on the therapeutic relevance of reactive oxygen and nitrogen species (RONS) in organs or on the impacts of activating and inhibiting haem oxygenase and nitric oxide synthase.
