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Chronic intermittent hypoxia-induced cardiovascular and renal dysfunction: from adaptation to maladaptation.
Arnaud, Claire; Billoir, Emma; de Melo Junior, Antonio F; Pereira, Sofia A; O'Halloran, Ken D; Monteiro, Emilia C.
Afiliación
  • Arnaud C; Université Grenoble-Alpes INSERM U1300, Laboratoire HP2, Grenoble, France.
  • Billoir E; Université Grenoble-Alpes INSERM U1300, Laboratoire HP2, Grenoble, France.
  • de Melo Junior AF; iNOVA4Health, NOVA Medical School, Universidade NOVA de Lisboa, Lisboa, Portugal.
  • Pereira SA; iNOVA4Health, NOVA Medical School, Universidade NOVA de Lisboa, Lisboa, Portugal.
  • O'Halloran KD; Department of Physiology, School of Medicine, College of Medicine & Health, University College Cork, Cork, Ireland.
  • Monteiro EC; iNOVA4Health, NOVA Medical School, Universidade NOVA de Lisboa, Lisboa, Portugal.
J Physiol ; 601(24): 5553-5577, 2023 Dec.
Article en En | MEDLINE | ID: mdl-37882783
Chronic intermittent hypoxia (CIH) is the dominant pathological feature of human obstructive sleep apnoea (OSA), which is highly prevalent and associated with cardiovascular and renal diseases. CIH causes hypertension, centred on sympathetic nervous overactivity, which persists following removal of the CIH stimulus. Molecular mechanisms contributing to CIH-induced hypertension have been carefully delineated. However, there is a dearth of knowledge on the efficacy of interventions to ameliorate high blood pressure in established disease. CIH causes endothelial dysfunction, aberrant structural remodelling of vessels and accelerates atherosclerotic processes. Pro-inflammatory and pro-oxidant pathways converge on disrupted nitric oxide signalling driving vascular dysfunction. In addition, CIH has adverse effects on the myocardium, manifesting atrial fibrillation, and cardiac remodelling progressing to contractile dysfunction. Sympatho-vagal imbalance, oxidative stress, inflammation, dysregulated HIF-1α transcriptional responses and resultant pro-apoptotic ER stress, calcium dysregulation, and mitochondrial dysfunction conspire to drive myocardial injury and failure. CIH elaborates direct and indirect effects in the kidney that initially contribute to the development of hypertension and later to chronic kidney disease. CIH-induced morphological damage of the kidney is dependent on TLR4/NF-κB/NLRP3/caspase-1 inflammasome activation and associated pyroptosis. Emerging potential therapies related to the gut-kidney axis and blockade of aryl hydrocarbon receptors (AhR) are promising. Cardiorenal outcomes in response to intermittent hypoxia present along a continuum from adaptation to maladaptation and are dependent on the intensity and duration of exposure to intermittent hypoxia. This heterogeneity of OSA is relevant to therapeutic treatment options and we argue the need for better stratification of OSA phenotypes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sistema Cardiovascular / Apnea Obstructiva del Sueño / Hipertensión Límite: Humans Idioma: En Revista: J Physiol Año: 2023 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sistema Cardiovascular / Apnea Obstructiva del Sueño / Hipertensión Límite: Humans Idioma: En Revista: J Physiol Año: 2023 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido