ArticleReproductive sciences (Thousand Oaks, Calif.)2014
Maternal high-salt intake during pregnancy reprogrammed renin-angiotensin system-mediated cardiomyocyte apoptosis in the adult offspring heart.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Mitochondrial Damage and Hypertension: Another Dark Side of Sodium Excess.Current nutrition reports · 2023Review
- Excessive Sodium Intake Leads to Cardiovascular Disease by Promoting Sex-Specific Dysfunction of Murine Heart.Frontiers in nutrition · 2022Article
- Increased exposure to sodium during pregnancy and lactation changes basal and induced behavioral and neuroendocrine responses in adult male offspring.Physiological reports · 2017Article
- Mitochondrial-dependent mechanisms are involved in angiotensin II-induced apoptosis in dopaminergic neurons.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2016Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
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Abstract
aimsExcess salt intake during pregnancy may alter fetal organ structures and functions leading to increased risks in the development of cardiovascular diseases in later life. The present study determined whether and how the prenatal high-salt (HS) diets affect renin-angiotensin system (RAS) that may mediate cardiac cell death. METHODS AND
resultsAngiotensin II receptors, AT1 and AT2, protein expression was increased in the myocardium of the offspring exposed to prenatal HS; apoptotic cells appeared in the myocardium of the adult offspring. Mitochondrion was isolated in cell experiments, and the data showed cardiomyocyte apoptosis requiring cytochrome C release. Pretreating H9C2 cells with AT2 agonist CGP42112A induced cell apoptosis in DNA fragments and activated caspase 3. CGP42112A increased mitochondrion cytochrome C release and apoptosis in the cells.
conclusionBoth in vitro and in vivo study demonstrated that cardiomyocyte apoptosis was related to AT2 activation. Prenatal HS diets may reprogram RAS that mediates apoptosis in the offspring myocardium, and AT2 may contribute to cardiomyocyte apoptosis via the cytochrome C release pathway.
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