ReviewBasic research in cardiology2023
Perspective: mitochondrial STAT3 in cardioprotection.
Review in Basic research in cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
- Inflammaging and cytokine-driven cardiovascular senescence in age-related myocardial infarction: mechanisms, biomarkers, and precision immunotherapy strategies.Biogerontology · 2026Review
- STAT Signaling in Metabolic Disorders: From Molecular Mechanisms to Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Insights in ischemia/reperfusion injury and cardioprotection: neglected and emerging pathways and therapeutic targets for a personalized therapy.Basic research in cardiology · 2026Review
- Preemptive cardioprotection with a small molecule in rodents that suppresses genes predictive of heart failure.Science advances · 2026Article
- Review
- RNF220 mediates K63-linked polyubiquitination of STAT3 and aggravates pathological cardiac hypertrophy.Cell death and differentiation · 2026Article
- Desidustat's cardioprotective mechanisms in heart failure: a network pharmacology, molecular docking and dynamics approach.Scientific reports · 2026Article
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- Remote ischemic conditioning protects against anthracycline cardiotoxicity without impairing its antitumor activity.Basic research in cardiology · 2026Article
- Mitochondrial Resilience: Unraveling the Triadic Interplay of Phosphocreatine, Cyclophilin D, and STAT3 in Heart Failure.Journal of cardiovascular translational research · 2026Review
- Causal relevance of the JAK/STAT pathway for cardioprotection via cold acclimation.Scientific reports · 2026Article
- Molecular and Cellular Mechanisms of Myocardial Ischemia and Reperfusion Injury: A Narrative Review.Cells · 2026Review
- Article
- Oxycodone: A Pain-Relieving Agent With Cardioprotective Properties Against Myocardial Ischemia-Reperfusion Injury.Cardiovascular therapeutics · 2026Review
- Cardioprotective Signaling: Outline and Future Directions.Biomedicines · 2025Review
- Inhibition of DYRK1B BY C81 impedes inflammatory processes in leukocytes by reducing STAT3 activity.Cellular and molecular life sciences : CMLS · 2025Article
- Cardioprotection of voluntary exercise against breast cancer-induced cardiac injury via STAT3.Basic research in cardiology · 2025Article
- Cardioprotection strategies for anthracycline cardiotoxicity.Basic research in cardiology · 2025Review
- MicroRNA-197-3p Transfection: Variations in Cardiomyocyte Gene Expression with Anaesthetics Drugs in a Model of Hypoxia/Reperfusion.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The Enigmata of Cardioprotection With SGLT2 Inhibition.JACC. Basic to translational science · 2025Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of signal transducer and activator of transcription 3 (STAT3) has been identified as a key cardioprotective signal not only in animal studies but also in humans-in animals, STAT3 is causally involved in cardioprotection. In response to late ischemic conditioning, canonical function of STAT3 activation upregulates the expression of cardioprotective and anti-apoptotic proteins. In its non-canonical function, STAT3 is activated during ischemic conditioning and is part of the cardioprotective cytosolic survival activating factor enhancement pathway. Activated STAT3 is imported and localized to the mitochondria. Mitochondrial STAT3 stimulates the activity of mitochondrial electron transport chain complex I, reduces mitochondrial reactive oxygen species production and mitochondrial permeability transition pore opening. Finally, two novel aspects of STAT activation in cardioprotection are discussed: a genetic variance of the STAT encoding region as a potential primordial confounding variable for cardioprotection, and the cardioprotective potential of sodium-glucose cotransporter 2 inhibitors through STAT3 activation.
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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 Socratic graph.