Frataxin-deficient cardiomyocytes present an altered thiol-redox state which targets actin and pyruvate dehydrogenase
Friedreich ataxia (FA) is a cardioneurodegenerative disease caused by deficient frataxin expression. This mitochondrial protein has been related to iron homeostasis, energy metabolism, and oxidative stress. Previously, we set up a cardiac cellular model of FA based on neonatal rat cardiac myocytes (...
Main Authors: | Rosa Purroy, Marta Medina-Carbonero, Joaquim Ros, Jordi Tamarit |
---|---|
Format: | Article |
Language: | English |
Published: |
Elsevier
2020-05-01
|
Series: | Redox Biology |
Online Access: | http://www.sciencedirect.com/science/article/pii/S2213231719315150 |
Similar Items
-
Nitric oxide prevents Aft1 activation and metabolic remodeling in frataxin-deficient yeast
by: David Alsina, et al.
Published: (2018-04-01) -
Cofilin dysregulation alters actin turnover in frataxin-deficient neurons
by: Diana C. Muñoz-Lasso, et al.
Published: (2020-03-01) -
Flavin adenine dinucleotide rescues the phenotype of frataxin deficiency.
by: Pilar Gonzalez-Cabo, et al.
Published: (2010-01-01) -
Mechanism by which insulin regulates pyruvate dehydrogenase activity in mitochondria
by: Yu-Chun Lin, et al.
Published: (2007) -
Pyruvate Dehydrogenase Kinase 4 Deficiency and Hepatic Steatosis
by: Hwang, Byounghoon
Published: (2009)