ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012
Akt and MAPK signaling mediate pregnancy-induced cardiac adaptation.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Guidelines for assessing maternal cardiovascular physiology during pregnancy and postpartum.American journal of physiology. Heart and circulatory physiology · 2024Guideline
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Maternal exercise is associated with enhanced systolic reserve and altered mitochondrial respiration in adult female offspring.American journal of physiology. Heart and circulatory physiology · 2026Article
- Antiretroviral therapy in the peripartum period impairs post pregnancy cardiac reverse remodeling in a rodent model.Nature communications · 2026Article
- Review
- mTORC1 and nuclear ERK spatially control translation in cardiomyocytes through 4EBP1 phosphorylation.Science signaling · 2026Article
- Cardiovascular complications of pregnancy.The Journal of clinical investigation · 2026Review
- Progesterone signaling in cardio-renal physiology and pathophysiology.Frontiers in endocrinology · 2026Review
- Peptidyl-tRNA hydrolase 2 is a negative regulator of peripartum cardiomyopathy with heart failure in female mice.Nature communications · 2025Article
- Calcium Signaling and Cardiac Adaptation to Stress: Focus on Pregnancy and Diabetes.Biomolecules · 2025Review
- Article
- Gestational arsenite exposure alters maternal postpartum heart size and induces CaAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- Maternal cardiovascular research and education should be prioritized in the United States.American journal of physiology. Heart and circulatory physiology · 2025Article
- Regression of postprandial cardiac hypertrophy in burmese pythons is mediated by FoxO1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Prenatal arsenite exposure alters maternal cardiac remodeling during late pregnancy.Toxicology and applied pharmacology · 2024Article
- A Conserved Mechanism of Cardiac Hypertrophy Regression through FoxO1.bioRxiv : the preprint server for biology · 2024Article
- Coordinated Metabolic Responses Facilitate Cardiac Growth in Pregnancy and Exercise.Current heart failure reports · 2023Review
- Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.Nature reviews. Cardiology · 2023Review
- Chromogranin A: An Endocrine Factor of Pregnancy.International journal of molecular sciences · 2023Review
- Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although the signaling pathways underlying exercise-induced cardiac adaptation have been extensively studied, little is known about the molecular mechanisms that result in the response of the heart to pregnancy. The objective of this study was to define the morphological, functional, and gene expression patterns that define the hearts of pregnant mice, and to identify the signaling pathways that mediate this response. Mice were divided into three groups: nonpregnant diestrus control, midpregnancy, and late pregnancy. Both time points of pregnancy were associated with significant cardiac hypertrophy. The prosurvival signaling cascades of Akt and ERK1/2 were activated in the hearts of pregnant mice, while the stress kinase, p38, was decreased. Given the activation of Akt in pregnancy and its known role in cardiac hypertrophy, the hypertrophic response to pregnancy was tested in mice expressing a cardiac-specific activated (myristoylated) form of Akt (myrAkt) or a cardiac-specific constitutively active (antipathologic hypertrophic) form of its downstream target, glycogen synthase kinase 3β (caGSK3β). The pregnancy-induced hypertrophic responses of hearts from these mice were significantly attenuated. Finally, we tested whether pregnancy-associated sex hormones could induce hypertrophy and alter signaling pathways in isolated neonatal rat ventricular myocytes (NRVMs). In fact, progesterone, but not estradiol treatment increased NRVM cell size via phosphorylation of ERK1/2. Inhibition of MEK1 effectively blocked progesterone-induced cellular hypertrophy. Taken together, our study demonstrates that pregnancy-induced cardiac hypertrophy is mediated by activation of Akt and ERK1/2 pathways.
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