The TLR9-IFN-I-mediated inflammatory response contributes significantly to both ischemic and post-ischemic myocardial ischemia-reperfusion injury. HMGB1 and cfDNA released from ischemic myocardium activated the intra-myocardial TLR9 - IFN-I inflammatory pathway during ischemia and the extra-myocardial TLR9 - IFN-I inflammatory pathway during reperfusion. Hydroxychloroquine reduces production of IFN-I and attenuates myocardial IRI, likely by inhibiting the TLR9-IFN-I pathway.
Keyphrases
- toll like receptor
- inflammatory response
- immune response
- ischemia reperfusion injury
- cerebral ischemia
- dendritic cells
- left ventricular
- nuclear factor
- oxidative stress
- lipopolysaccharide induced
- lps induced
- acute myocardial infarction
- subarachnoid hemorrhage
- signaling pathway
- brain injury
- heart failure
- blood brain barrier
- coronary artery disease
- acute coronary syndrome