Clec4e-Receptor Signaling in Myocardial Repair After Ischemia-Reperfusion Injury
| العنوان: | Clec4e-Receptor Signaling in Myocardial Repair After Ischemia-Reperfusion Injury |
|---|---|
| المؤلفون: | Denise Veltman, Piet Claus, Ellen Caluwé, Maarten Vanhaverbeke, Uwe Himmelreich, Stefan Janssens, Peter Pokreisz, Peter Sinnaeve, Willy Gsell, Ming Wu, Hilde Gillijns |
| المصدر: | JACC: Basic to Translational Science |
| بيانات النشر: | ELSEVIER SCIENCE INC, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Pathology, PRR, pattern recognition receptor, TnT, troponin T, Angiogenesis, CAD, coronary artery disease, NS, not significant, DAMP, damage-associated molecular pattern, SMC, smooth muscle cell, MPO, myeloperoxidase, myocardial remodeling, Car3, carbonic anhydrase 3, Transcriptome, Myocyte, magnetic resonance imaging, CMC, cardiac myocyte, Cxcr2, CXC chemokine receptor 2, ANOVA, analysis of variance, STEMI, ST-segment elevation myocardial infarction, I/R, ischemia-reperfusion, ECM, extracellular matrix, LAD, left anterior descending coronary artery, medicine.symptom, Grk2, G protein–coupled receptor kinase 2, Cardiology and Cardiovascular Medicine, Extracellular matrix organization, medicine.medical_specialty, qRT-PCR, quantitative reverse transcription polymerase chain reaction, ischemia-reperfusion injury, Ischemia, Inflammation, Downregulation and upregulation, Cxcl2, CXC chemokine ligand 2, medicine, CLEC4E, LV, left ventricular, CLEC4E, C-type lectin domain family 4 member E, business.industry, medicine.disease, Efna2, ephrin A2, WT, wild-type, ESV, end-systolic volume, AMI, acute myocardial infarction, inflammation, RNA, ribonucleic acid, ACS, acute coronary syndrome, Preclinical Research, hs-TnI, high-sensitivity troponin I, business, Reperfusion injury, MRI, magnetic resonance imaging |
| الوصف: | Visual Abstract Highlights • The role of the CLEC4E during myocardial healing after ischemia-reperfusion injury is unknown. • CLEC4E deletion is associated with reduced cardiac injury, inflammation, and left ventricular structural and functional remodeling. • CLEC4E is a promising target to modulate myocardial inflammation and enhance repair after ischemia-reperfusion injury. Summary The bacterial C-type lectin domain family 4 member E (CLEC4E) has an important role in sterile inflammation, but its role in myocardial repair is unknown. Using complementary approaches in porcine, murine, and human samples, we show that CLEC4E expression levels in the myocardium and in blood correlate with the extent of myocardial injury and left ventricular (LV) functional impairment. CLEC4E expression is markedly increased in the vasculature, cardiac myocytes, and infiltrating leukocytes in the ischemic heart. Loss of Clec4e signaling is associated with reduced acute cardiac injury, neutrophil infiltration, and infarct size. Reduced myocardial injury in Clec4e–/– translates into significantly improved LV structural and functional remodeling at 4 weeks’ follow-up. The early transcriptome of LV tissue from Clec4e–/– mice versus wild-type mice reveals significant upregulation of transcripts involved in myocardial metabolism, radical scavenging, angiogenesis, and extracellular matrix organization. Therefore, targeting CLEC4E in the early phase of ischemia-reperfusion injury is a promising therapeutic strategy to modulate myocardial inflammation and enhance repair after ischemia-reperfusion injury. |
| وصف الملف: | Electronic-eCollection |
| اللغة: | English |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::59a46fac4ecaf99cf50513516da72175Test https://lirias.kuleuven.be/handle/123456789/680542Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....59a46fac4ecaf99cf50513516da72175 |
| قاعدة البيانات: | OpenAIRE |
| الوصف غير متاح. |