ArticlePloS one2014
Mitochondrial p38β and manganese superoxide dismutase interaction mediated by estrogen in cardiomyocytes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Insights in ischemia/reperfusion injury and cardioprotection: neglected and emerging pathways and therapeutic targets for a personalized therapy.Basic research in cardiology · 2026Review
- In vitro sex-specific function-structure relationship in neonatal rat cardiac monolayers.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Inhibition of Cardiac p38 Highlights the Role of the Phosphoproteome in Heart Failure Progression.ACS omega · 2025Article
- Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024Review
- Anthracycline cardiotoxicity is exacerbated by global p38β genetic ablation in a sexually dimorphic manner but unaltered by cardiomyocyte-specific p38α loss.American journal of physiology. Heart and circulatory physiology · 2023Article
- Sex Differences in Myocardial and Vascular Aging.Circulation research · 2022Review
- A Novel Role of Claudin-5 in Prevention of Mitochondrial Fission Against Ischemic/Hypoxic Stress in Cardiomyocytes.The Canadian journal of cardiology · 2021Article
- Sex Differences in Molecular Mechanisms of Cardiovascular Aging.Frontiers in aging · 2021Review
- Sex Differences in Cardiovascular Aging and Heart Failure.Current heart failure reports · 2020Review
- Sex and Gender Differences in Heart Failure.International journal of heart failure · 2020Review
- Sex Hormone Regulation of Proteins Modulating Mitochondrial Metabolism, Dynamics and Inter-Organellar Cross Talk in Cardiovascular Disease.Frontiers in cell and developmental biology · 2020Review
- Sex differences in cardiometabolic disorders.Nature medicine · 2019Review
- A temperature-dependent conformational shift in p38α MAPK substrate-binding region associated with changes in substrate phosphorylation profile.The Journal of biological chemistry · 2019Article
- Novel Noncatalytic Substrate-Selective p38α-Specific MAPK Inhibitors with Endothelial-Stabilizing and Anti-Inflammatory Activity.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Does Cimicifuga racemosa have the effects like estrogen on the sublingual gland in ovariectomized rats?Biological research · 2017Article
- The Role of Estrogen and Estrogen Receptors on Cardiomyocytes: An Overview.The Canadian journal of cardiology · 2016Review
- p38 MAP kinases in the heart.Gene · 2016Review
- Estrogen potentiates reactive oxygen species (ROS) tolerance to initiate carcinogenesis and promote cancer malignant transformation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Article
- Mitochondrial maintenance failure in aging and role of sexual dimorphism.Archives of biochemistry and biophysics · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsWhile etiology behind the observed acceleration of ischemic heart disease in postmenopausal women is poorly understood, collective scientific data suggest cardioprotective effects of the endogenous female sex hormone, estrogen. We have previously shown that 17β-estradiol (E2) protects cardiomyocytes exposed to hypoxia-reoxygenation (H/R) by inhibiting p38α - p53 signaling in apoptosis and activating pro-survival p38β mitogen activated protein kinase (p38β MAPK), leading to suppression of reactive oxygen species (ROS) post H/R. However, little is known about the mechanism behind the antioxidant actions of E2-dependent p38β. The aim of this study is to determine whether the cytoprotection by estrogen involves regulation of manganese superoxide dismutase (MnSOD), a major mitochondrial ROS scavenging enzyme, via cardiac p38β. METHODS AND
resultsWe identified mitochondrial p38β by immunocytochemistry and by immunoblotting in mitochondria isolated from neonatal cardiomyocytes of Sprague-Dawley rats. E2 facilitated the mitochondrial localization of the active form of the kinase, phosphorylated p38β (p-p38β). E2 also reduced the H/R-induced mitochondrial membrane potential decline, augmented the MnSOD activity and suppressed anion superoxide generation, while the dismutase protein expression remained unaltered. Co-immunoprecipitation studies showed physical association between MnSOD and p38β. p38β phosphorylated MnSOD in an E2-dependent manner in in-vitro kinase assays.
conclusionThis work demonstrates for the first time a mitochondrial pool of active p38β and E2-mediated phosphorylation of MnSOD by the kinase. The results shed light on the mechanism behind the cytoprotective actions of E2 in cardiomyocytes under oxidative stress.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.