ArticleAnnals of surgery2007
The PI3K/Akt pathway mediates the nongenomic cardioprotective effects of estrogen following trauma-hemorrhage.
Article in Annals of surgery, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 68 citations in OpenAlex.
- Mitochondria at the Heart of Sepsis: Mechanisms, Metabolism, and Sex Differences.International journal of molecular sciences · 2025Review
- Evaluating the neuroprotective effects of progesterone receptors on experimental traumatic brain injury: The PI3K/Akt pathway.Brain and behavior · 2023Article
- Comparison of acute kidney injury following brain death between male and female rats.Clinics (Sao Paulo, Brazil) · 2023Article
- An atlas of dynamic peripheral blood mononuclear cell landscapes in human perioperative anaesthesia/surgery.Clinical and translational medicine · 2022Article
- 17-estradiol nanoparticles influence inflammatory response of myocardial infarction possibly through downregulation of miR-302b.American journal of translational research · 2021Article
- RvE1 Attenuates Polymicrobial Sepsis-Induced Cardiac Dysfunction and Enhances Bacterial Clearance.Frontiers in immunology · 2020Article
- Differential Effects of Brain Death on Rat Microcirculation and Intestinal Inflammation: Female Versus Male.Inflammation · 2018Article
- The influence of sex steroid hormones on the response to trauma and burn injury.Burns & trauma · 2017Review
- G-protein-coupled receptor 30-mediated antiapoptotic effect of estrogen on spinal motor neurons following injury and its underlying mechanisms.Molecular medicine reports · 2015Article
- Inhibition of IκB Kinase Attenuates the Organ Injury and Dysfunction Associated with Hemorrhagic Shock.Molecular medicine (Cambridge, Mass.) · 2015Article
- Anti-Inflammatory and Organ-Protective Effects of Resveratrol in Trauma-Hemorrhagic Injury.Mediators of inflammation · 2015Review
- Estrogen fails to facilitate resuscitation from ventricular fibrillation in male rats.American journal of translational research · 2015Article
- 17β-estradiol suppresses lipopolysaccharide-induced acute lung injury through PI3K/Akt/SGK1 mediated up-regulation of epithelial sodium channel (ENaC) in vivo and in vitro.Respiratory research · 2014Article
- Review
- Gender dimorphism of the cardiac dysfunction in murine sepsis: signalling mechanisms and age-dependency.PloS one · 2014Article
- 17β-estradiol confers protection after traumatic brain injury in the rat and involves activation of G protein-coupled estrogen receptor 1.Journal of neurotrauma · 2013Article
- The effects of estrogen on various organs: therapeutic approach for sepsis, trauma, and reperfusion injury. Part 1: central nervous system, lung, and heart.Journal of anesthesia · 2012Review
- Nontranscriptional activation of PI3K/Akt signaling mediates hypotensive effect following activation of estrogen receptor β in the rostral ventrolateral medulla of rats.Journal of biomedical science · 2012Article
- The toll-like receptor 9 agonist, CpG-oligodeoxynucleotide 1826, ameliorates cardiac dysfunction after trauma-hemorrhage.Shock (Augusta, Ga.) · 2012Article
- Estrogen and the cardiovascular system.Pharmacology & therapeutics · 2012Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveTo determine whether the nongenomic actions of E2 have any beneficial effect on cardiac function following trauma-hemorrhage and whether those effects are mediated via the PI3K/Akt pathway. SUMMARY BACKGROUND DATA: Since studies suggest that both genomic and nongenomic pathways are involved in mediating the salutary effects of 17beta-estradiol (estradiol) following trauma-hemorrhage, we examined if the nongenomic effects of estradiol on cardiac function after trauma-hemorrhage involve the PI3K/Akt pathway.
methodsMale Sprague-Dawley rats ( approximately 300 g) underwent trauma-hemorrhage (mean blood pressure, 40 mm Hg for 90 min, then resuscitation). Estradiol conjugated to bovine serum albumin (BSA) (estradiol-BSA; 1 mg/kg estradiol) with or without estrogen receptor antagonist (ICI 182,780), PI3K inhibitor (Wortmannin), or vehicle was injected intravenously during resuscitation. At 2 hours after trauma-hemorrhage or sham operation, cardiac output, stroke volume, heart rate, mean arterial pressure, and +/-dP/dt were measured. Cardiomyocyte PI3K, p-Akt, Akt protein expressions and apoptosis were also determined. One-way ANOVA and Tukey's test were used for statistical analysis.
resultsCardiac output, stroke volume, and +/-dP/dt decreased significantly after trauma-hemorrhage. Administration of estradiol or estradiol-BSA significantly improved these parameters of cardiac function. Although trauma-hemorrhage decreased cardiomyocyte PI3K protein expression and Akt phosphorylation (p-Akt), estradiol or estradiol-BSA treatment following trauma-hemorrhage prevented such decreases in cardiomyocyte PI3K protein expressions and p-Akt. The increase in cardiomyocyte apoptosis was also prevented in rats receiving estradiol-BSA. Co-administration of ICI 182,780 or Wortmannin abolished beneficial effects of estradiol-BSA on cardiac functions following trauma-hemorrhage.
conclusionThe PI3K/Akt pathway plays a critical role in mediating the nongenomic salutary effects of estradiol on cardiac function following trauma-hemorrhage.
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