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  1. The Neonatal Myeloid Hypoxia Response Promotes a Cardiac Regenerative Response through Insulin-Like Growth Factor
  2. Machine Learning Identifies Distinct Treg-Mediated Remodeling in HFpEF Hearts Treated with Neonatal Mesenchymal Stem Cells and Their Secretome
  3. Correction to: Myeloid Fatty Acid Metabolism Activates Neighboring Hematopoietic Stem Cells to Promote Heart Failure With Preserved Ejection Fraction
  4. LncRNA H19 Upregulation Links Hypoplastic Left Heart Syndrome to Impaired PINK1/Parkin-Mediated Mitophagy and Ischemic Vulnerability
  5. Myeloid Fatty Acid Metabolism Activates Neighboring Hematopoietic Stem Cells to Promote Heart Failure With Preserved Ejection Fraction
  6. Early-age efferocytosis directs macrophage arachidonic acid metabolism for tissue regeneration
  7. Mechanical regulation of macrophage metabolism by allograft inflammatory factor 1 leads to adverse remodeling after cardiac injury
  8. Leukocyte-lymphatic intersections during cardiac inflammation
  9. Hypoxia-inducible factor-2α enhances neutrophil survival to promote cardiac injury following myocardial infarction
  10. FOXC1 and FOXC2 Ablation Causes Abnormal Valvular Endothelial Cell Junctions and Lymphatic Vessel Formation in Myxomatous Mitral Valve Degeneration
  11. Genetic deletion or pharmacologic inhibition of histone deacetylase 6 protects the heart against ischaemia/reperfusion injury by limiting tumour necrosis factor alpha–induced mitochondrial injury in experimental diabetes
  12. Neonatal Cardiac Mesenchymal Stromal Cells Promote Recovery of Infarcted Myocardium through CD44 Mediated FoxP3+ T-Regulatory Cells after Vascular Infusion
  13. In Vivo Mapping of Myocardial Injury Outside the Infarct Zone: Tissue at an Intermediate Pathological State
  14. HSF-1 enhances cardioprotective potential of stem cells via exosome biogenesis and their miRNA cargo enrichment
  15. Augmentation of Histone Deacetylase 6 Activity Impairs Mitochondrial Respiratory Complex I in Ischemic/Reperfused Diabetic Hearts
  16. Cardio-omentopexy requires a cardioprotective innate immune response to promote myocardial angiogenesis in mice
  17. Wireless, implantable catheter-type oximeter designed for cardiac oxygen saturation
  18. Identification and analysis of circulating long non-coding RNAs with high significance in diabetic cardiomyopathy
  19. Genome-wide differential expression profiling of lncRNAs and mRNAs associated with early diabetic cardiomyopathy
  20. Current Status and Challenges of NRF2 as a Potential Therapeutic Target for Diabetic Cardiomyopathy
  21. Microarray analysis of long non-coding RNA and mRNA expression profiles in diabetic cardiomyopathy using human induced pluripotent stem cell–derived cardiomyocytes
  22. Current status and strategies of long noncoding RNA research for diabetic cardiomyopathy
  23. Vascular endothelial growth factor regulation of endothelial nitric oxide synthase phosphorylation is involved in isoflurane cardiac preconditioning
  24. Heme Oxygenase-1 Reduces Sepsis-Induced Endoplasmic Reticulum Stress and Acute Lung Injury
  25. Failure of Isoflurane Cardiac Preconditioning in Obese Type 2 Diabetic Mice Involves Aberrant Regulation of MicroRNA-21, Endothelial Nitric-oxide Synthase, and Mitochondrial Complex I
  26. The application of remote ischemic conditioning in heart surgery
  27. Transgenic overexpression of GTP cyclohydrolase 1 in cardiomyocytes ameliorates post-infarction cardiac remodeling
  28. Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy
  29. Cardiomyocyte GTP Cyclohydrolase 1 Protects the Heart Against Diabetic Cardiomyopathy
  30. Chronic Co-Administration of Sepiapterin and l -Citrulline Ameliorates Diabetic Cardiomyopathy and Myocardial Ischemia/Reperfusion Injury in Obese Type 2 Diabetic Mice
  31. MicroRNA-21 Mediates Isoflurane-induced Cardioprotection against Ischemia–Reperfusion Injury via Akt/Nitric Oxide Synthase/Mitochondrial Permeability Transition Pore Pathway
  32. Isoflurane Favorably Modulates Guanosine Triphosphate Cyclohydrolase-1 and Endothelial Nitric Oxide Synthase during Myocardial Ischemia and Reperfusion Injury in Rats
  33. Inhibition of PKCβ2 overexpression ameliorates myocardial ischaemia/reperfusion injury in diabetic rats via restoring caveolin-3/Akt signaling
  34. Up-regulation of MicroRNA-21 Mediates Isoflurane-induced Protection of Cardiomyocytes
  35. Far red/near infrared light-induced protection against cardiac ischemia and reperfusion injury remains intact under diabetic conditions and is independent of nitric oxide synthase
  36. Rap1b in Smooth Muscle and Endothelium Is Required for Maintenance of Vascular Tone and Normal Blood Pressure
  37. Impairment of Endothelial-Myocardial Interaction Increases the Susceptibility of Cardiomyocytes to Ischemia/Reperfusion Injury
  38. Apolipoprotein A-1 mimetic D-4F enhances isoflurane-induced eNOS signaling and cardioprotection during acute hyperglycemia
  39. 4F Decreases IRF5 Expression and Activation in Hearts of Tight Skin Mice
  40. Stress-Induced Cell-Cycle Activation in Tip60 Haploinsufficient Adult Cardiomyocytes
  41. Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning
  42. Characterization of a critical role for CFTR chloride channels in cardioprotection against ischemia/reperfusion injury
  43. Cardiac-specific overexpression of GTP cyclohydrolase 1 restores ischaemic preconditioning during hyperglycaemia
  44. A3 adenosine receptor activation during reperfusion reduces infarct size through actions on bone marrow-derived cells
  45. Cardiac myocyte-specific overexpression of human GTP cyclohydrolase I protects against acute cardiac allograft rejection
  46. Isoflurane Postconditioning Protects against Reperfusion Injury by Preventing Mitochondrial Permeability Transition by an Endothelial Nitric Oxide Synthase–dependent Mechanism
  47. Transient Receptor Potential Vanilloid Type 4–Deficient Mice Exhibit Impaired Endothelium-Dependent Relaxation Induced by Acetylcholine In Vitro and In Vivo
  48. The A3 Adenosine Receptor Agonist CP-532,903 [N6-(2,5-Dichlorobenzyl)-3′-aminoadenosine-5′-N-methylcarboxamide] Protects against Myocardial Ischemia/Reperfusion Injury via the Sarcolemmal ATP-Sensitive Potassium Channel
  49. Cl-IB-MECA [2-Chloro-N6-(3-iodobenzyl)adenosine-5′-N-methylcarboxamide] Reduces Ischemia/Reperfusion Injury in Mice by Activating the A Adenosine Receptor
  50. Improved cardiac function in infarcted mice after treatment with pluripotent embryonic stem cells
  51. Adenosine Inhibits Tumor Necrosis Factor-α Release from Mouse Peritoneal Macrophages via A2A and A2B but Not the A3 Adenosine Receptor
  52. Electrophysiologic and mechanical evidence of superiority of hyperpolarizing versus depolarizing cardioplegia in protection of endothelium-derived hyperpolarizing factor–mediated endothelial function: a study in coronary resistance arteries
  53. Comparison of Three Different A1 Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs
  54. A3adenosine receptor agonist IB-MECA reduces myocardial ischemia-reperfusion injury in dogs
  55. Comparison of Cardioprotective Efficacy of Two Thromboxane A2 Receptor Antagonists
  56. Cyclic ADP-Ribose Contributes to Contraction and Ca<sup>2+</sup> Release by M<sub>1</sub> Muscarinic Receptor Activation in Coronary Arterial Smooth Muscle
  57. Gene Dosage-Dependent Effects of Cardiac-Specific Overexpression of the A 3 Adenosine Receptor
  58. Myocardial ischemia and reperfusion reduce the levels of cyclic ADP-ribose in rat myocardium
  59. Role of ADP-ribose in 11,12-EET-induced activation of KCachannels in coronary arterial smooth muscle cells
  60. Difference in Endothelium-Derived Hyperpolarizing Factor–Mediated Hyperpolarization and Nitric Oxide Release Between Human Internal Mammary Artery and Saphenous Vein
  61. Difference in Endothelium-Derived Hyperpolarizing Factor-Mediated Hyperpolarization and Nitric Oxide Release Between Human Internal Mammary Artery and Saphenous Vein
  62. Effect of nitric oxide on calcium-induced calcium release in coronary arterial smooth muscle
  63. Endothelium-dependent hyperpolarization and relaxation resistance to NG-nitro-?-arginine and indomethacin in coronary circulation
  64. Altered endothelium-derived hyperpolarizing factor–mediated endothelial function in coronary microarteries by St Thomas' hospital solution