Post-TTM Rebound Pyrexia after Ischemia-Reperfusion Injury Results in Sterile Inflammation and Apoptosis in Cardiomyocytes.
Giang TongNalina N A von GarlenSylvia J WowroPhuong D LamJana KrechFelix BergerKatharina R L SchmittPublished in: Mediators of inflammation (2019)
Our findings show that maintaining a period of post-TTM "therapeutic normothermia" is effective in preventing secondary apoptosis-driven myocardial cell death, thus minimizing the infarct area and further release of mediators of the innate sterile inflammatory response after acute IR injury.
Keyphrases
- cell death
- oxidative stress
- cell cycle arrest
- ischemia reperfusion injury
- inflammatory response
- endoplasmic reticulum stress
- immune response
- acute myocardial infarction
- pi k akt
- lipopolysaccharide induced
- left ventricular
- toll like receptor
- lps induced
- cell proliferation
- heart failure
- endothelial cells
- percutaneous coronary intervention