Disfunción endotelial renal y estrés oxidativo en la obesidadpapel de la proteína quinasa activada por AMP (AMPK)

  1. Rodriguez Prados, Claudia
Supervised by:
  1. Dolores Prieto Ocejo Director
  2. Cristina Contreras Jiménez Director
  3. Luis Rivera de los Arcos Director

Defence university: Universidad Complutense de Madrid

Fecha de defensa: 04 October 2021

Committee:
  1. María Soledad Fernández Alfonso Chair
  2. Ana Alejandra Sanchez Pina Secretary
  3. Ramaroson Andriantsitohaina Committee member
  4. Marta Gil Ortega Committee member
  5. Miguel Antonio López Pérez Committee member

Type: Thesis

Abstract

AMPK is a key cellular energy sensor that is activated in energy deficiency states to stimulate catabolic pathways such as glycolysis and β-oxidation of fatty acids and thus obtain ATP that ensures homeostasis and cell survival (Hardie et al., 2016). In addition to its role in metabolism, AMPK participates in the regulation of autophagy (Alers et al., 2012), mitochondrial biogenesis (Zong et al., 2002) and vascular function (Salt & Hardie, 2017). AMPK is also involved in the regulation of ROS production derived from NADPH oxidases and mitochondria in the vasculature (Wang et al., 2012), as well as in the modulation of vascular inflammation (Katerelos et al., 2010).The kidney is an organ with a high metabolic rate and energy consumption. AMPK is abundantly expressed in the kidney and is implicated in the regulation of tubular transport, lipids and glucose metabolism and podocyte function, among many other functions (Hallows KR, 2010). However, its role in the renal vasculature is unknown...