Q3138713 (Q3138713): Difference between revisions
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(Created claim: summary (P836): Acute myocardial infarction (AMI) is a major health problem in the scenario of cardiovascular diseases in our society. Despite the measures available in the clinic, the mortality rate after AMI remains worrying, so in order to improve the prognosis of these patients it is necessary to implement the development of new lines of research focused on the study of the pathophysiology of AMI. To this end, the present project proposes to analyse the rol...) |
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Acute myocardial infarction (AMI) is a major health problem in the scenario of cardiovascular diseases in our society. Despite the measures available in the clinic, the mortality rate after AMI remains worrying, so in order to improve the prognosis of these patients it is necessary to implement the development of new lines of research focused on the study of the pathophysiology of AMI. To this end, the present project proposes to analyse the role of receptors of the immune system NOD1 (nucleotide binding oligomerisation domain containing 1) in the diagnosis, prognosis and treatment of AMI. Through a multidisciplinary study, we will analyse the NOD1 signaling pathway in myocardial samples and peripheral blood monocytes from healthy individuals and AMI patients. We will also evaluate the relationship between the degree of activation of this mediator and the heart damage and dysfunction associated with AMI. At the cellular level, we will study in human ventricular cardiomyocytes as different conditions of ischemia/reperfusion modulate the activation of NOD1. Currently, advances in the regeneration of the injured myocardium have focused on the application of gene therapy techniques through the use of stem cells. In this sense, using human mesenchymal stem cells, we will determine how NOD1 is able to regulate the regenerative capacity of the myocardium. Finally, we will evaluate how the genetic deficiency of NOD1 (Knock out NOD1-/-) affects adverse remodeling and cardiac dysfunction that occur after AMI in a murine experimental model. In short, the present translational study will determine whether NOD1 can be a new clinical biomarker of cardiac damage and emerge as a therapeutic target in the treatment of AMI. (English) | |||||||||||||||
| Property / summary: Acute myocardial infarction (AMI) is a major health problem in the scenario of cardiovascular diseases in our society. Despite the measures available in the clinic, the mortality rate after AMI remains worrying, so in order to improve the prognosis of these patients it is necessary to implement the development of new lines of research focused on the study of the pathophysiology of AMI. To this end, the present project proposes to analyse the role of receptors of the immune system NOD1 (nucleotide binding oligomerisation domain containing 1) in the diagnosis, prognosis and treatment of AMI. Through a multidisciplinary study, we will analyse the NOD1 signaling pathway in myocardial samples and peripheral blood monocytes from healthy individuals and AMI patients. We will also evaluate the relationship between the degree of activation of this mediator and the heart damage and dysfunction associated with AMI. At the cellular level, we will study in human ventricular cardiomyocytes as different conditions of ischemia/reperfusion modulate the activation of NOD1. Currently, advances in the regeneration of the injured myocardium have focused on the application of gene therapy techniques through the use of stem cells. In this sense, using human mesenchymal stem cells, we will determine how NOD1 is able to regulate the regenerative capacity of the myocardium. Finally, we will evaluate how the genetic deficiency of NOD1 (Knock out NOD1-/-) affects adverse remodeling and cardiac dysfunction that occur after AMI in a murine experimental model. In short, the present translational study will determine whether NOD1 can be a new clinical biomarker of cardiac damage and emerge as a therapeutic target in the treatment of AMI. (English) / rank | |||||||||||||||
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| Property / summary: Acute myocardial infarction (AMI) is a major health problem in the scenario of cardiovascular diseases in our society. Despite the measures available in the clinic, the mortality rate after AMI remains worrying, so in order to improve the prognosis of these patients it is necessary to implement the development of new lines of research focused on the study of the pathophysiology of AMI. To this end, the present project proposes to analyse the role of receptors of the immune system NOD1 (nucleotide binding oligomerisation domain containing 1) in the diagnosis, prognosis and treatment of AMI. Through a multidisciplinary study, we will analyse the NOD1 signaling pathway in myocardial samples and peripheral blood monocytes from healthy individuals and AMI patients. We will also evaluate the relationship between the degree of activation of this mediator and the heart damage and dysfunction associated with AMI. At the cellular level, we will study in human ventricular cardiomyocytes as different conditions of ischemia/reperfusion modulate the activation of NOD1. Currently, advances in the regeneration of the injured myocardium have focused on the application of gene therapy techniques through the use of stem cells. In this sense, using human mesenchymal stem cells, we will determine how NOD1 is able to regulate the regenerative capacity of the myocardium. Finally, we will evaluate how the genetic deficiency of NOD1 (Knock out NOD1-/-) affects adverse remodeling and cardiac dysfunction that occur after AMI in a murine experimental model. In short, the present translational study will determine whether NOD1 can be a new clinical biomarker of cardiac damage and emerge as a therapeutic target in the treatment of AMI. (English) / qualifier | |||||||||||||||
point in time: 12 October 2021
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Revision as of 13:19, 12 October 2021
Project Q3138713 in Spain
| Language | Label | Description | Also known as |
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| English | No label defined |
Project Q3138713 in Spain |
Statements
51,000.0 Euro
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102,000.0 Euro
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50.0 percent
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1 January 2018
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31 March 2021
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FUNDACION INVESTIGACION BIOMEDICA HOSPITAL LA PAZ
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40°25'0.12"N, 3°42'12.89"W
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28079
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El infarto agudo de miocardio (IAM) supone un problema sanitario importante en el escenario de las enfermedades cardiovasculares de nuestra sociedad. A pesar de las medidas disponibles en la clínica, el índice de mortalidad tras un IAM sigue siendo preocupante, por lo que para mejorar el pronóstico de estos pacientes es necesario implementar el desarrollo de nuevas líneas de investigación centradas en el estudio de la fisiopatología del IAM. Con este fin, el presente Proyecto propone analizar el papel que juegan los receptores del sistema inmune innato NOD1 (nucleotide binding oligomerization domain containing 1) en el diagnóstico, pronóstico y tratamiento del IAM. Mediante un estudio multidisciplinar, vamos a analizar la vía de señalización de NOD1 en muestras miocárdicas y en monocitos de sangre periférica de individuos sanos y de pacientes con IAM. Además evaluaremos la relación existente entre el grado de activación de este mediador y el daño y disfunción cardiaca asociados al IAM. A nivel celular, estudiaremos en cardiomiocitos ventriculares humanos como distintas condiciones de isquemia/reperfusión modulan la activación de NOD1. Actualmente, los avances en regeneración del miocardio lesionado se han centrado en la aplicación de técnicas de terapia génica mediante el uso de células madre. En este sentido, empleando células madre mesenquimales humanas, vamos a determinar cómo NOD1 es capaz de regular la capacidad regeneradora del miocardio. Por último, vamos a evaluar como la deficiencia genética de NOD1 (Knock out NOD1-/-) afecta al remodelado adverso y la disfunción cardiaca que tienen lugar tras un IAM en un modelo experimental murino. En definitiva, el presente estudio traslacional va a determinar si NOD1 puede ser un nuevo biomarcador clínico de daño cardiaco y surgir como una diana terapéutica en el tratamiento del IAM. (Spanish)
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Acute myocardial infarction (AMI) is a major health problem in the scenario of cardiovascular diseases in our society. Despite the measures available in the clinic, the mortality rate after AMI remains worrying, so in order to improve the prognosis of these patients it is necessary to implement the development of new lines of research focused on the study of the pathophysiology of AMI. To this end, the present project proposes to analyse the role of receptors of the immune system NOD1 (nucleotide binding oligomerisation domain containing 1) in the diagnosis, prognosis and treatment of AMI. Through a multidisciplinary study, we will analyse the NOD1 signaling pathway in myocardial samples and peripheral blood monocytes from healthy individuals and AMI patients. We will also evaluate the relationship between the degree of activation of this mediator and the heart damage and dysfunction associated with AMI. At the cellular level, we will study in human ventricular cardiomyocytes as different conditions of ischemia/reperfusion modulate the activation of NOD1. Currently, advances in the regeneration of the injured myocardium have focused on the application of gene therapy techniques through the use of stem cells. In this sense, using human mesenchymal stem cells, we will determine how NOD1 is able to regulate the regenerative capacity of the myocardium. Finally, we will evaluate how the genetic deficiency of NOD1 (Knock out NOD1-/-) affects adverse remodeling and cardiac dysfunction that occur after AMI in a murine experimental model. In short, the present translational study will determine whether NOD1 can be a new clinical biomarker of cardiac damage and emerge as a therapeutic target in the treatment of AMI. (English)
12 October 2021
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Madrid
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Identifiers
PI17_01344
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