Cardiac Ischemia and Reperfusion

This study shows ischemic postconditioning reduces cardiomyocyte apoptosis by inhibiting the RAP2C-MAP4K4 pathway, suggesting it as a therapeutic target for ischemic heart disease.

This study shows that Ffar4 and ChemR23 signaling in cardiac myocytes protects against ischemic injury by reducing oxidative stress and cell death.

This study shows L-lactic acid reduces myocardial infarct size and improves cardiac function through MCT1 transport, metabolic reprogramming, and gene expression changes in both acute and chronic settings.

This study examines inflammatory and transcriptomic changes in the myocardium of mice after cardiac arrest, finding increased neutrophils and cytokines that resolve over time, correlating with improved cardiac function.

This study shows that NRG-1 postconditioning protects against myocardial I/R injury by activating mitophagy through the UCP2/PINK1/LC3B pathway in rats and H9C2 cells.

This study investigates the role of neutrophil-specific STING in myocardial ischemia/reperfusion injury, finding that its deletion worsens cardiac function and alters immune cell responses.

This study shows that the DJ-1-derived peptide ND-13 reduces myocardial infarct size and preserves cardiac function by inhibiting mitochondrial fission and improving mitochondrial bioenergetics through the RhoA-ROCK1-Drp1 pathway.

This study uses RNA-Seq to analyze how remote ischaemic conditioning affects gene expression in a rat model of Necrotising enterocolitis, identifying suppressed pro-inflammatory pathways and potential therapeutic mechanisms.

This study investigates how remote ischemic conditioning affects inflammatory and metabolic pathways in mice, identifying specific plasma metabolites and showing protection against cerebral ischemia-reperfusion injury.

The paper shows that complement C3 interacts with cytochrome c in cardiomyocytes during heart ischemia/reperfusion, reducing apoptosis by sequestering cytochrome c.

This study shows that temporarily inhibiting protein translation after heart attack reduces inflammation and improves long-term heart function by targeting the mTORC1-4EBP1-eIF4F pathway.

This study identifies DISC1 as a key molecule for cardiomyocyte resilience after myocardial infarction, showing its role in cardioprotection through interaction with GSK3β and its relevance in cardiac health following coronary artery bypass grafting.

This study shows electro-acupuncture protects against myocardial I/R injury through STAT3 activation, not STAT5.

This study shows that once delayed non-invasive RIPC reduces brain injury and inflammation in rats after short-term reperfusion but not long-term reperfusion.

The paper identifies sex-specific gene expression changes in human myocardial tissue after ischemia, highlighting differences in pathways and cell-type proportions between males and females.