Leo Timmers

Cyclooxygenase-2 inhibition increases mortality, enhances left ventricular remodeling, and impairs systolic function after myocardial infarction in the pig.

Growth factor therapy in atherosclerotic disease-friend or foe.

Microsomal prostaglandin E2 synthase: a safer target than cyclooxygenases?

Toll-like receptor 4 mediates maladaptive left ventricular remodeling and impairs cardiac function after myocardial infarction.

Bridging innate immunity and myocardial ischemia/reperfusion injury: the search for therapeutic targets.

The Nuclear Factor-kappa B p50 subunit is involved in flow-induced outward arterial remodeling.

Targeted deletion of nuclear factor kappaB p50 enhances cardiac remodeling and dysfunction following myocardial infarction.

Exenatide reduces infarct size and improves cardiac function in a porcine model of ischemia and reperfusion injury.

Reduction of myocardial infarct size by human mesenchymal stem cell conditioned medium.

Myocardial ischemia/reperfusion injury is mediated by leukocytic toll-like receptor-2 and reduced by systemic administration of a novel anti-toll-like receptor-2 antibody.

Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury.

Arteriogenesis requires toll-like receptor 2 and 4 expression in bone-marrow derived cells.

Assessment of collateral artery function and growth in a pig model of stepwise coronary occlusion.

Human mesenchymal stem cell-conditioned medium improves cardiac function following myocardial infarction.

Effect of additional treatment with EXenatide in patients with an Acute Myocardial Infarction (EXAMI): study protocol for a randomized controlled trial.

The innate immune response in reperfused myocardium.

Treatment with OPN-305, a humanized anti-Toll-Like receptor-2 antibody, reduces myocardial ischemia/reperfusion injury in pigs.

Effect of additional treatment with EXenatide in patients with an Acute Myocardial Infarction: the EXAMI study.

Lack of haptoglobin results in unbalanced VEGFα/angiopoietin-1 expression, intramural hemorrhage and impaired wound healing after myocardial infarction.

Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury.

Taking risk prediction to the next level. Advances in biomarker research for atherosclerosis.

Microvesicle protein levels are associated with increased risk for future vascular events and mortality in patients with clinically manifest vascular disease.

Optical coherence tomography imaging of acute stent thrombosis after Stentys stent implantation.

Serum extracellular vesicle protein levels are associated with acute coronary syndrome.

Systemic toll-like receptor and interleukin-18 pathway activation in patients with acute ST elevation myocardial infarction.

Leucocyte expression of complement C5a receptors exacerbates infarct size after myocardial reperfusion injury.

Fast assessment and management of chest pain without ST-elevation in the pre-hospital gateway: rationale and design.

Very late bioresorbable vascular scaffold thrombosis following discontinuation of antiplatelet therapy.

Suspected acute coronary syndrome in the emergency room: Limited added value of heart type fatty acid binding protein point of care or ELISA tests: The FAME-ER (Fatty Acid binding protein in Myocardial infarction Evaluation in the Emergency Room) study.

BLT1 antagonist LSN2792613 reduces infarct size in a mouse model of myocardial ischaemia-reperfusion injury.

The diagnostic and prognostic potential of plasma extracellular vesicles for cardiovascular disease.

Ethnic differences in clinical outcome of patients presenting to the emergency department with chest pain.

Extracellular Vesicle Proteins Associated with Systemic Vascular Events Correlate with Heart Failure: An Observational Study in a Dyspnoea Cohort.

Coronary aneurysm without malapposition after bioresorbable vascular scaffold implantation.

No benefit of additional treatment with exenatide in patients with an acute myocardial infarction.