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

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Tytuł:: Nox4 Knockout Does Not Prevent Diaphragm Atrophy, Contractile Dysfunction, or Mitochondrial Maladaptation in the Early Phase Post-Myocardial Infarction in Mice.
Autorzy:: Hahn D; Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, FL, USA.
Kumar RA; Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, FL, USA.
Muscato DR; Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, FL, USA.
Ryan TE; Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, FL, USA.
Schröder K; Institute for Cardiovascular Physiology, Goethe University, Frankfurt, Germany.
Ferreira LF; Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, FL, USA, .
Źródło:: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology [Cell Physiol Biochem] 2021 Aug 20; Vol. 55 (4), pp. 489-504.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Publication: 2019- : Düsseldorf, Germany : Cell Physiol Biochem Press GmbH & Co KG
Original Publication: Basel ; New York : S. Karger, 1991-2018.
MeSH Terms:: Muscle Contraction*
Diaphragm/*enzymology
Mitochondria, Muscle/*enzymology
Muscular Atrophy/*enzymology
Myocardial Infarction/*enzymology
NADPH Oxidase 4/*deficiency
Animals ; Diaphragm/pathology ; Male ; Mice ; Mice, Knockout ; Mitochondria, Muscle/genetics ; Mitochondria, Muscle/pathology ; Muscular Atrophy/genetics ; Muscular Atrophy/pathology ; Myocardial Infarction/genetics ; Myocardial Infarction/pathology ; NADPH Oxidase 4/metabolism
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Grant Information:: R01 HL130318 United States HL NHLBI NIH HHS; R01 HL149704 United States HL NHLBI NIH HHS
Contributed Indexing:: Keywords: Atrophy; Oxidants; Force; Respiration; Heart failure
Substance Nomenclature:: EC 1.6.3.- (NADPH Oxidase 4)
EC 1.6.3.- (Nox4 protein, mouse)
Entry Date(s):: Date Created: 20210820 Date Completed: 20210930 Latest Revision: 20230511
Update Code:: 20240104
PubMed Central ID:: PMC10167972
DOI:: 10.33594/000000400
PMID:: 34416105
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Background/aims: 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.
Methods: We used wild-type (WT) and whole-body Nox4 knockout (Nox4KO) mice to measure diaphragm bundle force in vitro with a force transducer, mitochondrial respiration in isolated fiber bundles with an O 2 sensor, mitochondrial ROS by fluorescence, mRNA (RT-PCR) and protein (immunoblot), and fiber size by histology 72 hrs post-MI.
Results: MI decreased diaphragm fiber cross-sectional area (CSA) (~15%, p = 0.015) and maximal specific force (10%, p = 0.005), and increased actin carbonylation (5-10%, p = 0.007) in both WT and Nox4KO. Interestingly, MI did not affect diaphragm mRNA abundance of MAFbx/atrogin-1 and MuRF-1 but Nox4KO decreased it by 20-50% (p < 0.01). Regarding the mitochondria, MI and Nox4KO decreased the protein abundance of citrate synthase and subunits of electron transport system (ETS) complexes and increased mitochondrial O 2 flux (JO 2 ) and H 2 O 2 emission (JH 2 O 2 ) normalized to citrate synthase. Mitochondrial electron leak (JH 2 O 2 /JO 2 ) in the presence of ADP was lower in Nox4KO and not changed by MI.
Conclusion: Our study shows that the early phase post-MI causes diaphragm atrophy, contractile dysfunction, sarcomeric actin oxidation, and decreases citrate synthase and subunits of mitochondrial ETS complexes. These factors are potential causes of loss of inspiratory muscle strength and endurance in patients, which likely contribute to the pathophysiology in the early phase post-MI. Whole-body Nox4KO did not prevent the diaphragm abnormalities induced 72 hrs post-MI, suggesting that systemic pharmacological inhibition of Nox4 will not benefit patients in the early phase post-MI.
Competing Interests: The authors declare they have no conflict of interests.
(© Copyright by the Author(s). Published by Cell Physiol Biochem Press.)

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