Nox4 Knockout Does Not Prevent Diaphragm Atrophy, Contractile Dysfunction, or Mitochondrial Maladaptation in the Early Phase Post-Myocardial Infarction in Mice

• Published in: Cellular physiology and biochemistry Vol. 55; no. 4; pp. 489 - 504
• Main Authors: Hahn, Dongwoo, Kumar, Ravi A, Muscato, Derek R, Ryan, Terence E, Schröder, Katrin, Ferreira, Leonardo F
• Format: Journal Article
• Language: English
• Published: Germany Cell Physiol Biochem Press GmbH & Co KG 20.08.2021
• Subjects: Animals; Diaphragm - enzymology; Diaphragm - pathology; Male; Mice; Mice, Knockout; Mitochondria, Muscle - enzymology; Mitochondria, Muscle - genetics; Mitochondria, Muscle - pathology; Muscle Contraction; Muscular Atrophy - enzymology; Muscular Atrophy - genetics; Muscular Atrophy - pathology; Myocardial Infarction - enzymology; Myocardial Infarction - genetics; Myocardial Infarction - pathology; NADPH Oxidase 4 - deficiency; NADPH Oxidase 4 - metabolism; Atrophy; Oxidants; Force; Respiration; Heart failure

Diaphragm dysfunction with increased reactive oxygen species (ROS) occurs within 72 hrs post-myocardial infarction (MI) in mice and may contribute to loss of inspiratory maximal pressure and endurance in patients. We used wild-type (WT) and whole-body Nox4 knockout (Nox4KO) mice to measure diaphragm...