Project Details
Projekt
H2S-induced modulation of the trauma response in nicotine-induced COPD and diabetes (B02)
Subject Area
Anaesthesiology
Orthopaedics, Traumatology, Reconstructive Surgery
Orthopaedics, Traumatology, Reconstructive Surgery
Term
from 2015 to 2022
Project identifier
Deutsche Forschungsgemeinschaft (DFG) - Project number 251293561
This project demonstrated that deletion of the H2S-producing enzyme cystathionine--lyase (CSE) exacerbated acute lung injury after blunt chest trauma, in particular, in the presence of cigarette smoke exposure-induced COPD. Pre-traumatic cigarette smoke exposure also aggravated kidney (AKI) and lung (ALI) injury after combined blunt chest trauma and HS. COPD frequently coincides with diabetes, which in turn induces CSE down-regulation. Therefore, B02 hypothesizes that diabetes aggravates AKI and ALI injury after combined blunt chest trauma and HS in COPD, which is further enhanced by CSE deletion. We expect that exogenous H2S attenuates organ injury via reduced radical formation and improved mitochondrial function.
DFG Programme
Collaborative Research Centres
Subproject of
SFB 1149:
Danger Response, Disturbance Factors and Regenerative Potential after Acute Trauma
Applicant Institution
Universität Ulm
