ArticleInternational journal of cardiology2019
Long-term exposure to high altitude hypoxia during pregnancy increases fetal heart susceptibility to ischemia/reperfusion injury and cardiac dysfunction.
Article in International journal of cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 29 citations in OpenAlex.
- Fetal programming of the cardiac mitochondrial permeability transition pore in male offspring from hypoxic pregnancies.Redox biology · 2026Article
- Article
- Determinants of Place of Delivery Among Migrant Working Mothers in China.International journal of women's health · 2025Article
- Nicotinamide Riboside, an NAD + Precursor, Protects Against Cardiac Mitochondrial Dysfunction in Fetal Guinea Pigs Exposed to Gestational Hypoxia.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Astragaloside IV attenuates cardiac hypertrophy in rats born from mothers with intrauterine hypoxia through the PKCβII/Egr‑1 pathway.Experimental and therapeutic medicine · 2023Article
- Inhibition of DNA methylation in newborns reprograms ischemia-sensitive biomarkers resulting in development of a heart ischemia-sensitive phenotype late in life.Reproductive toxicology (Elmsford, N.Y.) · 2021Article
- Impact of intrauterine hypoxia on adolescent and adult cognitive function in rat offspring: sexual differences and the effects of spermidine intervention.Acta pharmacologica Sinica · 2021Article
- Sex differences and the effects of intrauterine hypoxia on growth and in vivo heart function of fetal guinea pigs.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- SUMOylation-Mediated Response to Mitochondrial Stress.International journal of molecular sciences · 2020Review
- Article
- High altitude exposure during pregnancy enhances the vulnerability of fetal heart dysfunction to ischemic stress: Epigenetic mechanisms.International journal of cardiology · 2019Article
- Spermidine Prevents Heart Injury in Neonatal Rats Exposed to Intrauterine Hypoxia by Inhibiting Oxidative Stress and Mitochondrial Fragmentation.Oxidative medicine and cellular longevity · 2019Article
- Epigenetic Down-Regulation of Sirt 1 via DNA Methylation and Oxidative Stress Signaling Contributes to the Gestational Diabetes Mellitus-Induced Fetal Programming of Heart Ischemia-Sensitive Phenotype in Late Life.International journal of biological sciences · 2019Article
- The cardiovascular system and high-altitude exposure: from adaptation to disease. Part I.Archivos peruanos de cardiologia y cirugia cardiovascularArticle
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8 authors at 2 institutions in 2 countries.
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Abstract
backgroundHigh altitude hypoxia (HAH) exposure affects fetal development. However, the fetal cardiovascular responses to the HAH are not well understood. We have tested the hypothesis that long-term HAH exposure alters the hypoxia/ischemia-sensitive gene expressions, leading to an increase in fetal heart susceptibility to ischemia/reperfusion (I/R) injury and cardiac dysfunction.
methodsTime-dated pregnant sheep were exposed to high-altitude (3820 m) or were maintained at sea level (~300 m) for 110 days. Fetal hearts were isolated from the near-term ewes and subjected to I/R in a Langendorff preparation.
resultsHAH decreased the fetal body and heart weights in the female but not male fetuses. HAH had no effect on the left ventricle (LV) function at baseline, but increased the LV infarct size and attenuated the post-ischemic recovery of LV function in both male and female fetuses, as compared with the normoxic groups. HAH increased the protein levels of hypoxia-inducible factor (HIF)-1α and DNA methyltransferases type 3b (DNMT3b), but attenuated protein kinase C epsilon (PKCε) levels in the fetal hearts. AHA induced a 4.3 fold increase of miR-210 in the males and a 2.9 fold increase in female hearts. In addition, HAH had no effect on mTOR protein and phosphorylation levels but increased the autophagy biomarker, LC3B-II protein levels and LC3B-II/LC3B-I ratio in the fetal hearts.
conclusionThe results suggest that gestational HAH exposure induces in utero programming of the hypoxia/ischemia-sensitive gene expression pattern in the developing heart and increases cardiac susceptibility to I/R injury.
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