ReviewJournal of molecular medicine (Berlin, Germany)2019
Connecting sex differences, estrogen signaling, and microRNAs in cardiac fibrosis.
Review in Journal of molecular medicine (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 63 citations in OpenAlex.
- BCKDK protects against obesity-induced cardiac remodelling and dysfunction by alleviating mitochondrial oxidative stress and ROS-driven MAPK signalling.Redox biology · 2026Article
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Development and validation of a predictive scoring model for post-ESD coagulation syndrome in elderly with colorectal LSTs.International journal of colorectal disease · 2026Article
- Tectochrysin alleviates Ang II-induced pathological cardiac hypertrophy by binding to STING and inhibiting STING/NFκB-mediated inflammation.Frontiers in pharmacology · 2026Article
- Cardiomyocyte-derived OTUD7B promotes cardiac hypertrophy by deubiquitinating SERCA2a.Theranostics · 2026Article
- The Role of MicroRNAs in the Pathophysiology and Management of Heart Failure: From Molecular Mechanisms to Clinical Application.International journal of molecular sciences · 2025Review
- Review
- Exploring sex differences in myocardial fibrosis in patients with structurally normal hearts.Scientific reports · 2025Article
- Cardiovascular risk of gender-affirming estrogen therapy in a transgender rat model.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Multi-microRNA diagnostic panel for heart failure with preserved ejection fraction in preclinical and clinical settings.ESC heart failure · 2025Article
- Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 and inducing mitochondrial dysfunction.Nature communications · 2025Article
- Computational modelling of cardiac fibroblast signalling reveals a key role for CaThe Journal of physiology · 2025Article
- Estrogen attenuates stiffness-driven fibrotic signaling via transcriptional regulation.Biophysical journal · 2025Article
- Sex-dependent Pathophysiology and Therapeutic Considerations in Right Heart Disease.The Canadian journal of cardiology · 2025Review
- Hormone Replacement Therapy and Cardiovascular Health in Postmenopausal Women.International journal of molecular sciences · 2025Review
- Ovarian Aging: The Silent Catalyst of Age-Related Disorders in Female Body.Aging and disease · 2025Review
- Sex in cardiovascular disease: Why this biological variable should be considered in in vitro models.Science advances · 2024Review
- Cardiac Left Ventricular miRNA-26a Is Downregulated in Ovariectomized Mice, Upregulated upon 17-Beta Estradiol Replacement, and Inversely Correlated with Collagen Type 1 Gene Expression.International journal of molecular sciences · 2024Article
- Sex differences in the association between epicardial adipose tissue volume and left atrial volume index.BMC cardiovascular disorders · 2024Article
- TXNIP aggravates cardiac fibrosis and dysfunction after myocardial infarction in mice by enhancing the TGFB1/Smad3 pathway and promoting NLRP3 inflammasome activation.Acta biochimica et biophysica Sinica · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Sex differences are evident in the pathophysiology of heart failure (HF). Progression of HF is promoted by cardiac fibrosis and no fibrosis-specific therapies are currently available. The fibrotic response is mediated by cardiac fibroblasts (CFs), and a central event is their phenotypic transition to pro-fibrotic myofibroblasts. These myofibroblasts may arise from various cellular origins including resident CFs and epicardial and endothelial cells. Both female subjects in clinical studies and female animals in experimental studies generally present less cardiac fibrosis compared with males. This difference is at least partially considered attributable to the ovarian hormone 17β-estradiol (E2). E2 signals via estrogen receptors to regulate genes are involved in the fibrotic response and myofibroblast transition. Besides protein-coding genes, E2 also regulates transcription of microRNA that modulate cardiac fibrosis. Sex dimorphism, E2, and miRNAs form multi-level regulatory networks in the pathophysiology of cardiac fibrosis, and the mechanism of these networks is not yet fully deciphered. Therefore, this review is aimed at summarizing current knowledge on sex differences, E2, and estrogen receptors in cardiac fibrosis, emphasizing on microRNAs and myofibroblast origins. KEY MESSAGES: • E2 and ERs regulate cardiac fibroblast function. • E2 and ERs may distinctly affect male and female cardiac fibrosis pathophysiology. • Sex, E2, and miRNAs form multi-level regulatory networks in cardiac fibrosis. • Sex-dimorphic and E2-regulated miRNAs affect mesenchymal transition.
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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.