ReviewFrontiers in cardiovascular medicine2019
STAT3 and Endothelial Cell-Cardiomyocyte Dialog in Cardiac Remodeling.
Review in Frontiers in cardiovascular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Epigenetic regulation by HDAC11-driven STAT3 activation promotes pro-inflammatory cytokine production and endothelial dysfunction upon bacterial infection in diabetes.Cell communication and signaling : CCS · 2026Article
- The role of LNK in mitigating hypertension: inhibition of vascular smooth muscle proliferation and JAK-STAT pathway.Molecular and cellular biochemistry · 2025Article
- Sex difference in human diseases: mechanistic insights and clinical implications.Signal transduction and targeted therapy · 2024Review
- Integrative Bioinformatics Approaches to Uncover Hub Genes and Pathways Involved in Cardiovascular Diseases.Cell biochemistry and biophysics · 2024Article
- Shock drives a STAT3 and JunB-mediated coordinated transcriptional and DNA methylation response in the endothelium.Journal of cell science · 2023Article
- Mitochondria in endothelial cells angiogenesis and function: current understanding and future perspectives.Journal of translational medicine · 2023Review
- Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling.Cell death discovery · 2023Article
- Impact of blood factors on endothelial cell metabolism and function in two diverse heart failure models.PloS one · 2023Article
- Updated Perspectives on Direct Vascular Cellular Reprogramming and Their Potential Applications in Tissue Engineered Vascular Grafts.Journal of functional biomaterials · 2022Review
- Regulation of the Tec family of non-receptor tyrosine kinases in cardiovascular disease.Cell death discovery · 2022Review
- Leucine-rich repeat kinase-2 deficiency protected against cardiac remodelling in mice via regulating autophagy formation and degradation.Journal of advanced research · 2022Article
- Article
- Slc39a2-Mediated Zinc Homeostasis Modulates Innate Immune Signaling in Phenylephrine-Induced Cardiomyocyte Hypertrophy.Frontiers in cardiovascular medicine · 2021Article
- Human pluripotent stem cell-derived cardiac stromal cells and their applications in regenerative medicine.Stem cell research · 2020Review
- Hypoxia-Inducible Factor-1α: The Master Regulator of Endothelial Cell Senescence in Vascular Aging.Cells · 2020Review
- Effects of Cardiomyocyte-Specific Deletion of STAT3-A Murine Model of Heart Failure With Preserved Ejection Fraction.Frontiers in cardiovascular medicine · 2020Article
- PTX3 Predicts Myocardial Damage and Fibrosis in Duchenne Muscular Dystrophy.Frontiers in physiology · 2020Article
- A novel role of miR-223-3p in reducing NLRP3-mediated inflammation and deep vein thrombosis in a mouse model.Science progressArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This article presents an overview of the central role of STAT3 in the crosstalk between endothelial cells and cardiac myocytes in the heart. Endothelial cell STAT3 has a key role in inflammation that underlies cardiovascular disease and impacts on cardiac structure and function. STAT3 in endothelial cells contributes to adverse cardiomyocyte genetic reprograming, for instance, during peripartum cardiomyopathy. Conversely, cardiomyocyte STAT3 is important for maintaining endothelial cell function and capillary integrity with aging and hypertension. In addition, STAT3 serves as a sentinel for stress in the heart. Recent evidence has revealed that the redox nature of STAT3 is regulated, and STAT3 is responsive to oxidative stress (ischemia-reperfusion) so as to induce protective genes. At the level of the mitochondrion, STAT3 is important in regulating reactive oxygen species (ROS) formation, metabolism, and mitochondrial integrity. STAT3 may also control calcium release from the ER so as to limit its subsequent uptake by mitochondria and the induction of cell death. Under normal conditions, some STAT3 localizes to intercalated discs of cardiomyocytes and serves to transmit pro-fibrotic gene induction signals in the nucleus with increased blood pressure. Further research is needed to understand how the sentinel role of STAT3 in both endothelial cells and cardiomyocytes is integrated in order to coordinate the response of the heart to both physiological and pathological demands.
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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.