Cardiac Ischemia and Reperfusion

AN INTEGRATED HEART-ON-A-CHIP NAM RESOLVES DISTINCT CLINICAL PHENOTYPES OF MYOCARDIAL ISCHEMIA-REPERFUSION INJURY

This paper develops a heart-on-a-chip model to distinguish structural, biochemical, and contractile changes in myocardial ischemia-reperfusion injury, linking them to distinct clinical phenotypes.

Cardiac unloading via a transvalvular pump prevents arrhythmias following myocardial ischemia / reperfusion by preserving coronary microcirculation and cardiomyocyte nanostructure

This study shows that transvalvular unloading reduces arrhythmias after myocardial ischemia/reperfusion by preserving coronary microcirculation and cardiomyocyte nanostructure in a porcine model.

Impact of GPR39 Inhibition on Tissue Oxygen Tension in Acute Myocardial Infarction: Modeling Using an Indirect Response Pharmacokinetics/Pharmacodynamics Approach

This paper develops a population PK/PD model to simulate the effects of VC108, a GPR39 inhibitor, on myocardial oxygen tension during acute myocardial infarction and reperfusion.

Caloric Restriction Promotes Ischemia/Reperfusion Cardioprotection Through Increased Mitochondrial Na+/Ca2+ Exchange

This study shows caloric restriction enhances mitochondrial Na+/Ca2+ exchange, reducing oxidative stress and improving cardiac recovery after ischemia/reperfusion injury.

TH1834-Mediated TIP60 Inhibition Protects Against Ischemia/Reperfusion Damage in Human iPSC-Derived Cardiomyocytes and Cardioids

This study shows that TH1834 inhibits TIP60, improving recovery in human iPSC-derived cardiomyocytes and cardioids after ischemia/reperfusion injury by enhancing metabolic flexibility and calcium homeostasis.

Selective Pharmacological Blockade of GPR39 Markedly Reduces No Reflow and Infarct Volumes in a Rat Acute Myocardial Infarction When Administered Prior to Reperfusion

Single intravenous bolus of the GPR39 antagonist VC108 shrank infarct and no-reflow volumes in rat myocardial infarction when given before reperfusion, but not 30 min after reperfusion.

Ablation of GM3 Gangliosides in cardiomyocytes modestly impacts heart size but does not protect the murine heart against ischemia reperfusion injury

This study shows that removing GM3 gangliosides in cardiomyocytes slightly reduces heart size but does not protect against ischemia-reperfusion injury.

Humanin analogue promotes metabolic reprogramming to protect the ischemic heart

This paper shows that a Humanin analogue improves cardiac function and reduces remodeling in ischemic hearts by promoting metabolic reprogramming from fatty acids to glucose.

CAD rewires nucleotide metabolism to drive oxidative stress in myocardial ischemia/reperfusion injury

This study identifies CAD as a key regulator of myocardial ischemia/reperfusion injury by linking nucleotide metabolism to oxidative stress through dual-compartment ROS signaling.

Mutation of a single cysteine in CaMKIIδ protects the heart from ischemia-reperfusion Injury

This study shows that mutating Cys273 in CaMKIIδ prevents disulfide formation, protecting the heart from ischemia-reperfusion injury without affecting normal cardiac function.

Formate reduces ischemic injury in the male heart by increasing protein S-nitrosation

This study shows formate reduces ischemic injury in male hearts by increasing protein S-nitrosation and preserving BH4 levels through a NOS-dependent mechanism.

Asporin Improves Cardiac Myocyte Response to Ischemia and Reperfusion Stress

This study investigates the protective effects of ASPN in cardiac myocytes under ischemia-reperfusion stress using an in vitro model, finding it modulates apoptosis, autophagy, and fibrosis-related pathways.

UBA1 Mitigates Myocardial Ischemia/Reperfusion Injury by Attenuating Endoplasmic Reticulum-Mitochondria Contacts via Pdzd8 ubiquitination

This study identifies UBA1 as a protective factor against myocardial ischemia/reperfusion injury by reducing endoplasmic reticulum-mitochondria contacts through Pdzd8 ubiquitination.

An inducer of snail hibernation causes quiescence and hibernation-like cardioprotection, through metabolic rewiring and autophagy, in mice hearts

This study identifies a hibernation-inducing factor from snails, SNAP, which induces quiescence and cardioprotection in mice hearts through metabolic rewiring and autophagy during ischemia-reperfusion injury.

In vivo imaging of reactive oxygen species after myocardial ischemia-reperfusion injury: a large animal multimodal imaging and transcriptomic study

This study uses multimodal imaging and transcriptomics to show increased reactive oxygen species activity in myocardial tissue and systemic organs after myocardial infarction, with associated gene expression changes.

Cardiac metabolite exchange measured in pigs during myocardial ischemia and reperfusion

This study measures cardiac metabolite exchange in pigs during myocardial ischemia and reperfusion, revealing dynamic metabolic changes and transient protein degradation.

Relaxation of cardiac pericytes by GLP-1 activating KATP channels mediates remote ischaemic preconditioning cardioprotection

This study shows that remote ischaemic preconditioning protects the heart by releasing GLP-1, which relaxes cardiac pericytes and reduces no-reflow.

VEGF-B/NRP1 Signaling Modulates Mitochondrial Homeostasis and Cardiac Function After Myocardial Infarction

This study investigates the protective role of VEGF-B/NRP1 signaling in cardiomyocytes after myocardial infarction, showing improved mitochondrial function and cardiac regeneration.

Synthetic torpor in the rat protects the heart from ischaemia-reperfusion injury

This study induces synthetic torpor in rats and shows it reduces heart damage from ischaemia-reperfusion injury by ~40%.

Peroxisome proliferator-activated receptor gamma (PPARG)-mediated myocardial salvage in acute myocardial infarction managed with left ventricular unloading and coronary reperfusion

This study investigates the mechanisms of myocardial salvage in acute myocardial infarction using left ventricular unloading and reperfusion, identifying PPARG as a key cardioprotective gene and suggesting rosiglitazone as a potential adjuvant therapy.

The Cardioprotective Effect of Ischemic Postconditioning is Mediated by Inhibiting RAP2C-MAP4K4 Pathway

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

A Cell Autonomous Free fatty acid receptor 4 - ChemR23 Signaling Cascade Protects Cardiac Myocytes from Ischemic Injury

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

L-lactic acid induces short- and long-term cardioprotective effects through MCT1 transport, induction of metabolic reprogramming, and gene expression modulation.

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.

Temporal dynamics of inflammatory and transcriptome changes in the myocardium in a murine model of cardiac arrest

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.

Neuregulin-1 Attenuates Myocardial Ischemia/Reperfusion Injury by Activating the UCP2/PINK1/LC3B-mediated Mitophagy

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.

The Cardioprotective Role of Neutrophil-Specific STING in Myocardial Ischemia/Reperfusion Injury

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.

The DJ-1-derived peptide, ND-13, confers cardioprotection by inhibiting mitochondrial fission and preserving mitochondrial bioenergetics via the RhoA-ROCK1-Drp1 pathway

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.

Remote ischemic conditioning modulates inflammatory response and metabolic pathways

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.

Complement C3 interacts with cytochrome c to influence myocardial apoptosis during heart ischemia/reperfusion

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

Transient inhibition of translation improves long-term cardiac function after ischemia/reperfusion by attenuating the inflammatory response

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.