title: Cardiotrophin-1 in hypertensive heart disease.
abstract: Hypertensive heart disease, here defined by the presence of pathologic left ventricular hypertrophy in the absence of a cause other than arterial hypertension, is characterized by complex changes in myocardial structure including enhanced cardiomyocyte growth and non-cardiomyocyte alterations that induce the remodeling of the myocardium, and ultimately, deteriorate left ventricular function and facilitate the development of heart failure. It is now accepted that a number of pathological processes mediated by mechanical, neurohormonal, and cytokine routes acting on the cardiomyocyte and the non-cardiomyocyte compartments are responsible for myocardial remodeling in the context of arterial hypertension. For instance, cardiotrophin-1 is a cytokine member of the interleukin-6 superfamily, produced by cardiomyocytes and non-cardiomyocytes in situations of biomechanical stress that once secreted interacts with its receptor, the heterodimer formed by gp130 and gp90 (also known as leukemia inhibitory factor receptor beta), activating different signaling pathways leading to cardiomyocyte hypertrophy, as well as myocardial fibrosis. Beyond its potential mechanistic contribution to the development of hypertensive heart disease, cardiotrophin-1 offers the opportunity for a new translational approach to this condition. In fact, recent evidence suggests that cardiotrophin-1 may serve as both a biomarker of left ventricular hypertrophy and dysfunction in hypertensive patients, and a potential target for therapies aimed to prevent and treat hypertensive heart disease beyond blood pressure control.
authors.affiliation: Área de Ciencias Cardiovasculares, Centro de Investigación Médica Aplicada, Universidad de Navarra, Av. Pío XII 55, 31008, Pamplona, Spain.
authors.forename: Arantxa
authors.initials: A
authors.lastname: González
authors.forename: Begoña
authors.initials: B
authors.lastname: López
authors.forename: Susana
authors.initials: S
authors.lastname: Ravassa
authors.forename: Javier
authors.initials: J
authors.lastname: Beaumont
authors.forename: Amaia
authors.initials: A
authors.lastname: Zudaire
authors.forename: Idoia
authors.initials: I
authors.lastname: Gallego
authors.forename: Cristina
authors.initials: C
authors.lastname: Brugnolaro
authors.forename: Javier
authors.initials: J
authors.lastname: Díez
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D002316:Cardiotonic Agents / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism / Q000502:physiology* / Q000627:therapeutic use; D006331:Heart Diseases / Q000175:diagnosis* / Q000209:etiology / Q000235:genetics / Q000628:therapy*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000175:diagnosis* / Q000235:genetics / Q000628:therapy; D008954:Models, Biological; D058990:Molecular Targeted Therapy / Q000379:methods
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D016207:Cytokines; C092073:cardiotrophin 1