Publications by authors named "K Grunz"
Background: Excess fibrotic remodeling causes cardiac dysfunction in ischemic heart disease, driven by MAP (mitogen-activated protein) kinase-dependent TGF-ß1 (transforming growth factor-ß1) activation by coagulation signaling of myeloid cells. How coagulation-inflammatory circuits can be specifically targeted to achieve beneficial macrophage reprogramming after myocardial infarction (MI) is not completely understood.
Methods: Mice with permanent ligation of the left anterior descending artery were used to model nonreperfused MI and analyzed by single-cell RNA sequencing, protein expression changes, confocal microscopy, and longitudinal monitoring of recovery.
Background: Accumulating evidence implicates the activation of G-protein-coupled PARs (protease-activated receptors) by coagulation proteases in the regulation of innate immune responses.
Methods: Using mouse models with genetic alterations of the PAR2 signaling platform, we have explored contributions of PAR2 signaling to infection with coxsackievirus B3, a single-stranded RNA virus provoking multiorgan tissue damage, including the heart.
Results: We show that PAR2 activation sustains correlates of severe morbidity-hemodynamic compromise, aggravated hypothermia, and hypoglycemia-despite intact control of the virus.
Antiphospholipid antibodies (aPL) in primary or secondary antiphospholipid syndrome (APS) are a major cause for acquired thrombophilia, but specific interventions preventing autoimmune aPL development are an unmet clinical need. Although autoimmune aPL cross react with various coagulation regulatory proteins, lipid-reactive aPL, including those derived from patients with COVID-19, recognize the endolysosomal phospholipid lysobisphosphatidic acid presented by the cell surface-expressed endothelial protein C receptor. This specific recognition leads to complement-mediated activation of tissue factor (TF)-dependent proinflammatory signaling and thrombosis.
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- Protease activated receptors (PARs) link blood clotting processes with immune responses, and PAR2 signaling, particularly involving tissue factor (TF) and factor VIIa (FVIIa), plays a crucial role in cancer cell movement and inflammation.
- Myeloid cells expressing FVII are important for recruiting inflammatory cells to the lungs after viral challenges, highlighting that a specific PAR2 cleavage pathway is essential for lung inflammation.
- The study reveals that through biased signaling involving β-arrestin, PAR2 mediates macrophage migration and immune recruitment to lung tissues, suggesting that targeting this signaling pathway could offer new treatment options for inflammation-related conditions.
Introduction: In spinal surgery, precise instrumentation is essential. This study aims to evaluate the accuracy of navigated, O-arm-controlled screw positioning in thoracic and lumbar spine instabilities.
Materials And Methods: Posterior instrumentation procedures between 2010 and 2015 were retrospectively analyzed.