ReviewFrontiers in cardiovascular medicine2015
Pivotal Importance of STAT3 in Protecting the Heart from Acute and Chronic Stress: New Advancement and Unresolved Issues.
Review in Frontiers in cardiovascular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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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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
47 citing papers in PubMed, 78 citations in OpenAlex.
- Nuclear Proteome Map of Mouse Heart Chambers.Molecular & cellular proteomics : MCP · 2026Article
- IL-10-STAT3-Dependent Transcriptional Regulation in Microglia: Alzheimer's Disease and Neuroinflammation.Biomedicines · 2026Review
- A mitochondrial regulatory network of ferroptosis defense in HPV-positive cervical cancer: therapeutic implications of the mitoSTAT3-DHODH axis.Frontiers in pharmacology · 2026Review
- Cyclophilin B deficiency enhances myocardial energy synthesis and protects against heart failure in preclinical models.BMC medicine · 2025Article
- STAT3 Protein-Protein Interaction Analysis Finds P300 as a Regulator of STAT3 and Histone 3 Lysine 27 Acetylation in Pericytes.Biomedicines · 2024Article
- The MEF2A transcription factor interactome in cardiomyocytes.Cell death & disease · 2023Article
- Intralipid® improves left ventricular function in rats with lipopolysaccharide-induced endotoxaemia by a Src-STAT3-mediated mechanism.British journal of anaesthesia · 2023Article
- BAM15 as a mitochondrial uncoupler: a promising therapeutic agent for diverse diseases.Frontiers in endocrinology · 2023Review
- Lack of STAT1 co-operative DNA binding protects against adverse cardiac remodelling in acute myocardial infarction.Frontiers in cardiovascular medicine · 2023Article
- Role of STAT3 and NRF2 in Tumors: Potential Targets for Antitumor Therapy.Molecules (Basel, Switzerland) · 2022Review
- Cardiac inducing colonies halt fibroblast activation and induce cardiac/endothelial cells to move and expand via paracrine signaling.Molecular biology of the cell · 2022Article
- Integrated analysis of miRNA-mRNA interaction in pediatric dilated cardiomyopathy.Pediatric research · 2022Article
- The crosstalk between STAT3 and microRNA in cardiac diseases and protection.Frontiers in cardiovascular medicine · 2022Review
- Bilateral Superior Cervical Sympathectomy Activates Signal Transducer and Activator of Transcription 3 Signal to Alleviate Myocardial Ischemia-Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Article
- Exploring the Communal Pathogenesis, Ferroptosis Mechanism, and Potential Therapeutic Targets of Dilated Cardiomyopathy and Hypertrophic CardiomyopathyFrontiers in cardiovascular medicine · 2022Article
- Emerging therapeutic targets for cardiac hypertrophy.Expert opinion on therapeutic targets · 2022Review
- Review
- Aging-Induced Impairment of Vascular Function: Mitochondrial Redox Contributions and Physiological/Clinical Implications.Antioxidants & redox signaling · 2021Review
- Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function.Basic research in cardiology · 2021Review
- Interferon γ neutralization reduces blood pressure, uterine artery resistance index, and placental oxidative stress in placental ischemic rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The transcription factor, signal transducer and activator of transcription 3 (STAT3), has been implicated in protecting the heart from acute ischemic injury under both basal conditions and as a crucial component of pre- and post-conditioning protocols. A number of anti-oxidant and antiapoptotic genes are upregulated by STAT3 via canonical means involving phosphorylation on Y705 and S727, although other incompletely defined posttranslational modifications are involved. In addition, STAT3 is now known to be present in cardiac mitochondria and to exert actions that regulate the electron transport chain, reactive oxygen species production, and mitochondrial permeability transition pore opening. These non-canonical actions of STAT3 are enhanced by S727 phosphorylation. The molecular basis for the mitochondrial actions of STAT3 is poorly understood, but STAT3 is known to interact with a critical subunit of complex I and to regulate complex I function. Dysfunctional complex I has been implicated in ischemic injury, heart failure, and the aging process. Evidence also indicates that STAT3 is protective to the heart under chronic stress conditions, including hypertension, pregnancy, and advanced age. Paradoxically, the accumulation of unphosphorylated STAT3 (U-STAT3) in the nucleus has been suggested to drive pathological cardiac hypertrophy and inflammation via non-canonical gene expression, perhaps involving a distinct acetylation profile. U-STAT3 may also regulate chromatin stability. Our understanding of how the non-canonical genomic and mitochondrial actions of STAT3 in the heart are regulated and coordinated with the canonical actions of STAT3 is rudimentary. Here, we present an overview of what is currently known about the pleotropic actions of STAT3 in the heart in order to highlight controversies and unresolved issues.
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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.