رسالة جامعية
Deciphering the Interlink between STAT3 and MAPKs in Ischemia/Reperfusion and Ischemic Conditioning ; Déchiffrer les Liens entre STAT3 et les MAPKs au course du Ischémie/Reperfusion et Postconditionnement Ischémique
| العنوان: | Deciphering the Interlink between STAT3 and MAPKs in Ischemia/Reperfusion and Ischemic Conditioning ; Déchiffrer les Liens entre STAT3 et les MAPKs au course du Ischémie/Reperfusion et Postconditionnement Ischémique |
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| المؤلفون: | Harhous, Zeina |
| المساهمون: | Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Lyon, École doctorale des Sciences et de Technologie (Beyrouth), Gabriel Bidaux, Mazen Kurdi |
| المصدر: | https://theses.hal.science/tel-03782027Test ; Tissues and Organs [q-bio.TO]. Université de Lyon; École doctorale des Sciences et de Technologie (Beyrouth), 2019. English. ⟨NNT : 2019LYSE1145⟩. |
| بيانات النشر: | HAL CCSD |
| سنة النشر: | 2019 |
| المجموعة: | HAL Lyon 1 (University Claude Bernard Lyon 1) |
| مصطلحات موضوعية: | STAT3, Myocardial Infarction, Ischemia/Reperfusion, Ischemic postconditioning, Infarctus myocarde, Postconditionnement ischémique, Ischémie-reperfusion, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO] |
| الوصف: | Cardiovascular diseases are leading causes of morbidity and mortality worldwide. Among the mostly prevailing cardiovascular diseases is myocardial infarction, which is pathologically defined as myocardial death due to a prolonged ischemia. Ischemia is an insufficient supply of blood caused by a blockade in the coronary arteries. The early restoration of blood flow is considered the most effective method against the ischemic lesions. Paradoxically, this blood flow restoration is associated with an exacerbation of the tissue injury, leading to the ischemia-reperfusion (I/R) injury. To avoid this injury, the myocardial ischemic conditioning protocol has rejuvenated the field of cardioprotection. This protocol confers its cardioprotective effects via recruiting various endogenous mechanisms following the activation of two intracellular pathways: the reperfusion injury salvage kinase (RISK) or survivor activator factor enhancer (SAFE) pathways. These pathways involve the activation of different signaling cascades and protein kinases. Zooming in through the SAFE pathway, the signal transducer and activator of transcription-3, STAT3, has been identified as a prominent key player in ischemic postconditioning (IPoC). The cardioprotective effects attributed to STAT3 are suggested to be linked to its roles as a transcription factor and as a regulator of the mitochondrial activity, but these are not well studied and elaborated. STAT3 is activated by phosphorylation, which targets the tyrosine 705 and serine 727 residues. In our current work, we initially aimed to investigate the mitochondrial cardioprotective roles of STAT3 following I/R and IPoC. However, we were not able to detect STAT3 in the mitochondria of adult mouse cardiomyocytes under variousbasal and stress conditions using different approaches. Interestingly, we showed an exclusive STAT3 pattern in adult cardiac myocytes, along the T-tubules, and highlighted drawbacks of previously used techniques. Aside from the mitochondrial roles of STAT3, we targeted its ... |
| نوع الوثيقة: | doctoral or postdoctoral thesis |
| اللغة: | English |
| العلاقة: | NNT: 2019LYSE1145; tel-03782027; https://theses.hal.science/tel-03782027Test; https://theses.hal.science/tel-03782027/documentTest; https://theses.hal.science/tel-03782027/file/TH2019HARHOUSZEINA.pdfTest |
| الإتاحة: | https://theses.hal.science/tel-03782027Test https://theses.hal.science/tel-03782027/documentTest https://theses.hal.science/tel-03782027/file/TH2019HARHOUSZEINA.pdfTest |
| حقوق: | info:eu-repo/semantics/OpenAccess |
| رقم الانضمام: | edsbas.1D1D5BF6 |
| قاعدة البيانات: | BASE |
| الوصف غير متاح. |