Cardiac Left Ventricle Mitochondrial Dysfunction After Neonatal Exposure to Hyperoxia: Relevance for Cardiomyopathy After Preterm Birth.
Adolescent
Adult
Animals
Cardiomyopathies
/ etiology
Female
Humans
Hyperoxia
/ complications
Intracellular Signaling Peptides and Proteins
/ blood
Male
Mitochondria
/ metabolism
Myocytes, Cardiac
/ metabolism
Oxidative Phosphorylation
Premature Birth
Rats
Rats, Sprague-Dawley
Ventricular Dysfunction, Left
/ etiology
Young Adult
cardiomyopathies
humanin
hyperoxia
mitochondria
premature birth
Journal
Hypertension (Dallas, Tex. : 1979)
ISSN: 1524-4563
Titre abrégé: Hypertension
Pays: United States
ID NLM: 7906255
Informations de publication
Date de publication:
03 2022
03 2022
Historique:
pubmed:
29
12
2021
medline:
3
3
2022
entrez:
28
12
2021
Statut:
ppublish
Résumé
Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm. Sprague-Dawley pups were exposed to room air (controls) or 80% O Compared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced In conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609.
Sections du résumé
BACKGROUND
Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm.
METHODS
Sprague-Dawley pups were exposed to room air (controls) or 80% O
RESULTS
Compared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced
CONCLUSIONS
In conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609.
Identifiants
pubmed: 34961326
doi: 10.1161/HYPERTENSIONAHA.121.17979
pmc: PMC8823906
doi:
Substances chimiques
Intracellular Signaling Peptides and Proteins
0
humanin
0
Banques de données
ClinicalTrials.gov
['NCT03261609']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
575-587Subventions
Organisme : CIHR
ID : 390615
Pays : Canada
Organisme : CIHR
ID : 133572
Pays : Canada
Organisme : CIHR
ID : 159688
Pays : Canada
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